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HE Encyclopedia of 



Poisons and 



Antidotes 



THIRD EDITION 



CAROL TURKINGTON 
DEBORAH MITCHELL 



THE ENCYCLOPEDIA OF 

POISONS AND 
ANTIDOTES 

Third Edition 



THE ENCYCLOPEDIA OF 



POISONS AND 
ANTIDOTES 

Third Edition 



Carol Turkington 
and 

Deborah Mitchell 



0 Facts On File 

An imprint oflnfobase Publishing 



The Encyclopedia of Poisons and Antidotes, Third Edition 

Copyright © 2010, 1999 by Estate of Carol Turkington 

All rights reserved. No part of this book may be reproduced or utilized in any form or by any means, 
electronic or mechanical, including photocopying, recording, or by any information storage or retrieval 
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Facts On File 
An imprint of Infobase Publishing 
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Library of Congress Cataloging-in-Publication Data 

Turkington, Carol. 

The encyclopedia of poisons and antidotes / Carol Turkington with Deborah Mitchell ; foreword by 

Shirley K. Osterhout. — 3rd ed. 
p. ; cm. — (Facts on File library of health and living) 
Rev. ed. of: The poisons and antidotes sourcebook. 2nd ed. cl999. 
Includes bibliographical references and index. 
ISBN-13: 978-0-8160-6401-4 (hardcover : alk. paper) 
ISBN-10: 0-8160-6401-6 (hardcover : alk. paper) 
1. Toxicological emergencies — Handbooks, manuals, etc. 2. Poisoning — Handbooks, manuals, etc. 
1. Mitchell, Deborah R. 11. Turkington, Carol. Poisons and antidotes sourcebook. III. Title. IV. Series: 

Facts on File library of health and living. 
[DNLM: 1. Poisons — Encyclopedias — English. 2. Antidotes — Encyclopedias — English. QV 13 T939e 2010] 

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CONTENTS 

Acknowledgments vii 

Introduction ix 

Entries A to Z 1 
Appendixes 

Appendix I: Home Testing Kits for Toxic Substances 276 

Appendix II: Hotlines 278 

Appendix III: Newsletters 279 

Appendix IV: Organizations 280 
Appendix V: Poison Education and Information Materials 284 

Appendix VI: Regional Poison Control Centers 288 

Appendix VII: Web Sites 294 

Glossary 296 

References 298 

Index 306 



ACKNOWLEDGMENTS 



The author would like to thank the librarians 
at the National Library of Medicine and the 
medical libraries of Hershey Medical Center, the 
University of Pennsylvania Medical Center and 
Reading Medical Center, the staffers at the National 
Institutes of Health and the countless people from 



national organizations, services, and government 
agencies around the country concerned with toxi- 
cology and poisons. A special thank you to Heather 
Albright and Catie Fisher for valuable Internet 
research assistance. 



vii 



INTRODUCTION 



>/ 'Y~l verything is poison, there is poison in 
li everything. Only the dose makes a thing 
not a poison." This quote, attributed to Paracelsus, 
the Swiss physician and alchemist born in 1493 
who has been called the father of toxicology, still 
rings true. It seems barely a day passes that we 
are not made aware of a new toxic substance that 
threatens our children or are informed by the 
media about the dangers of toxins found in our 
food, air, and water. Poisons and toxic substances 
are commonplace in everyday modern life. 

Yet poisons and other toxic substances have 
been a subject of fascination since ancient times. 
Archaeologists have found evidence that primitive 
humans used poisons with their hunting weapons 
to hasten the death of their prey. Humankind's 
great interest in poisons eventually extended to 
ways they could be used against their own kind, 
and this use bred a great deal of fear, especially 
among people in positions of power who were 
afraid that poisons would be used against them. 
One such individual was Mithridates VI, a king of 
Pontus in ancient northern Turkey about 114 B.C. 
He was so paranoid about being poisoned that he 
dedicated much of his life to finding antidotes to 
known toxic substances of his time. He left behind 
a wealth of notes about poisons and antidotes, 
including the 54 ingredients of an antidote he had 
concocted to ward off any attempts by his enemies 
to poison him. 

Leap ahead several millennia to the 2 1st century 
where people are exposed to literally tens of thou- 
sands of poisonous and toxic substances, with new 
ones being introduced all the time. Being poisoned 



today is often accidental and happens frequently 
in children, in whom poisoning is the fourth most 
common cause of death. Most accidental poison- 
ings can be prevented simply by keeping harmful 
substances out of the reach of children. Other 
cases of poisoning can be avoided with a healthful 
dose of knowledge and common sense, such as 
knowing which household chemicals should not 
be mixed, keeping certain plants away from pets, 
always wearing protective clothing when using 
pesticides or certain paint materials, and being 
aware of toxins in the home and other environ- 
ments that can cause insidious effects. Although 
antidotes are more available today than in the 
past and scientists are always working to develop 
new ones, prevention will always be better than 
treatment. 

This revised edition reflects many changes in 
the world of toxicology. Foremost is new research 
in the field that includes not only information on 
new toxic substances that can impact health but 
important, updated data on former entries. Among 
the many new entries are: 

• bisphenol: A potentially deadly toxin that is 
found not only in canned foods but in the ubiq- 
uitous water bottles and baby toys, including 
those children chew and suck on 

• flunitrazepam: Under the trade name of Rohyp- 
nol, it is commonly used as a date rape drug 

• mold: It has always been around, but in recent 
years it has become a huge health (and legal) 
concern when it is found in homes, schools, and 



ix 



X The Encyclopedia of Poisons and Antidotes 



other buildings. Black mold is associated with 
toxicity, but what about other common molds? 
We take a closer look. 

• polonium-210: A known poison that recently 
(2006) made headhnes when it was used to 
cause the demise of Russian dissident Alexan- 
der Litvinenko. Apparently this rare radioac- 
tive element is more accessible than previously 
thought. 

Many changes in toxicology have occurred over 
the past 10 years, so each of the original entries 
in this book has been reviewed and updated, as 
needed, with relevant information. This updated 
edition also has been partially reformatted to 
make it easier for readers to locate essential infor- 
mation. Thus the first 38 pages of the first edition, 
which covered critical topics such as "What To 
Do in a Poisoning Emergency," "How to Prevent 
Poisoning in Your Home," "How to Prevent Food 
Poisoning," and "Poisons by Symptom," have 
been incorporated into the A-to-Z format that 
makes up the rest of the book (except for the 
appendixes). 

As before, this book is designed as a guide and 
reference to a wide range of poisons and antidotes. 
It is not a substitute for prompt medical attention from 
a poison control center or an experienced physician 
trained in toxicology. All cases of suspected poison- 
ing should be reported immediately to a poison 
control center. 



Specific entries include poisonous and toxic sub- 
stances and their antidotes. All commonly encoun- 
tered poisonous and toxic substances, plants, and 
creatures have been included, together with a fair 
representation of more unusual varieties found 
throughout the world. 

To make information more accessible, entries 
relating to poisonous and toxic substances have been 
subdivided by category into "poisonous part" (where 
applicable), "symptoms," and "treatment." Entries 
are listed by common names, with Latin names in 
parentheses; additional common names or nick- 
names are also provided for all poisonous and toxic 
entries. All entries are extensively cross-referenced. 

Information in this book comes from the most 
up-to-date sources available and includes some of 
the most recent research in the field of toxicology, 
but readers should keep in mind that changes are 
occurring all the time. Although this book can 
serve as a comprehensive, concise, and convenient 
source of critical information, its format and space 
limitations do not allow it to address all the needs 
of its readers. Thus the appendixes, which have 
been updated extensively for this edition, provide 
the latest relevant information on home testing 
kits, hotlines, newsletters, organizations, poison 
control centers, sources of educational materials, 
and more — all for parents, teachers, health profes- 
sionals, and all other curious readers who want 
to keep their finger on the pulse of change in the 
extremely complex field of toxicology. 



ENTRIES A TO Z 



AAPCC Toxic Exposure Surveillance System 
(TESS) A method of collecting poison data from 
the American Association of Poison Control Cen- 
ters (AAPCC). This system, formerly known as 
the National Data Collection System, has grown 
steadily since its inception in 1983. TESS is the only 
comprehensive poisoning surveillance database in 
the United States and serves as a valuable resource 
for product safety managers, medical directors, and 
regulatory affairs directors. 

TESS contains detailed toxicological information 
on all human poison exposures reported to U.S. 
poison centers. The database is updated daily, with 
approximately 6,500 new cases added each day, or 
more than 2.3 million per year. Approximately 44 
percent of cases are followed up to determine the 
course and outcome of the exposure. 

acetaminophen This widely used painkiller is also 
known as paracetamol or by its chemical name, 
N-acetyl-p-aminophenol (APAP). Acetaminophen 
is sold under the trade names Tylenol, Tempra, 
or Panadol and generally is not poisonous unless 
ingested in large amounts — usually accidentally 
by children, as a means to commit suicide, or 
inadvertently when combined wdth various cough 
and cold medications, many of which also con- 
tain acetaminophen. Some of those medications 
include hydrocodone with acetaminophen (Lortab, 
Vicodin), tramadol with acetaminophen (Ultracet), 
propoxyphene (Darvocet), oxycodone (Percocet), 
pamabrom, pyrilamine (Midol, Pamprin), and Tyle- 
nol with codeine. 

Although researchers are still unsure about the 
key to APAP's painkilling action, it is known that 
the drug can damage the kidney and liver when 
taken in excessive amounts. Research suggests that 



combined with even small amounts of alcohol, 
APAP can cause liver toxicity. 

Symptoms 

If a toxic dose has been taken, symptoms will appear 
within 24 to 36 hours and include nausea, vomiting, 
abdominal pain, lethargy, and jaundice at 48 hours 
or later. The minimum toxic dose in adults in a single 
ingestion is 7.5-10 grams; in children younger than 
12 years it is 150 milligrams/kilograms. Chronic tox- 
icity among alcoholics has been reported after daily 
ingestion of high doses (5-6 grams). 

Treatment 

Empty the stomach as soon as possible by lavage 
or with syrup of ipecac. Specific treatment is deter- 
mined by a blood level of the drug after four hours. 
The specific antidote is N-acetylcysteine (NAC), 
which, for maximum liver protection, should be 
given within eight to 10 hours of ingesting acet- 
aminophen. NAC is given in 17 doses in a hospital. 
Provide general supportive care for kidney or liver 
failure; liver transplant may be necessary. 

acetylcysteine Antidote for acetaminophen over- 
dose and possibly for carbon tetrachloride and 
chloroform poisoning. Acetylcysteine often causes 
nausea and vomiting when given by mouth. In rare 
cases, generalized urticaria has been observed in 
patients receiving oral acetylcysteine. If this occurs 
or other allergic symptoms appear, acetylcysteine 
treatment should be stopped. If the drug is vom- 
ited, it should be given again. Rapid intravenous 
administration can cause a drop in blood pressure, 
and at least one death has been reported when a 
child received a rapid intravenous dose. 
See also acetaminophen. 



1 



2 acids 



acids Acids are chemical substances that have a 
sour taste, are soluble in water, and turn litmus 
paper red. They produce pain and corrosion to all 
tissues with which they come in contact. Prob- 
lems in swallowing, nausea, intense thirst, shock, 
breathing problems, and death can result from 
ingesting acids. 

Acid poisonings should be treated hke any other 
poisoning emergency: Give the person fluids to 
drink and call the poison control center for specific 
instructions. DO NOT INDUCE VOMITING. 

Acids are identified by their pH value, which 
ranges from 0 to 14; acidic substances are listed 
from strongest (0) to weakest (6). Neutral pH is 7; 
8 through 14 are alkaline (base). 

Many of the foods we eat and drink are slightly 
acid or base, as are our body's fluids. One of the 
most common acids is vitamin C (ascorbic acid). 
Others include 

• sulfuric acid: found in automobile batteries, 
metal cleaners, and polishes 

• hydrochloric acid: metal cleaners and polishes 

• nitric acid: cleaning solutions 

• oxalic acid: cleaning solutions, furniture and 
floor polishes, waxes, and bleach 

• phosphoric acid: metal cleaners and polishes 

• carbolic acid or phenol: antiseptics, disinfectants, 
preservatives 

See also dimethyl sulfate; phenol. 
aconite See monkshood. 



aconitine The chief active ingredient in the dried, 
powdered root of monkshood (aconite). Aconitine 
is an unstable alkaloid used in some liniments. 

Symptoms 

This central nervous system stimulant causes a 
burning sensation of the mouth, tongue, lips, and 
throat nearly immediately after ingestion. Other 
symptoms include nausea, vomiting, diarrhea, 
restlessness, vertigo, slow breathing, low body tem- 
perature, and convulsions. As little as two to five 



milhgrams (approximately one teaspoonful of the 
root) may cause death from paralysis of the cardiac 
muscle or respiratory system. 

Treatment 

Symptomatic. There are separate reports that amio- 
darone and magnesium sulphate may be effective 
in suppressing ventricular tachyarrhythmia (fast 
rhythm in the heart's lower chambers) caused by 
aconitine toxicity. 

See also monkshood. 



acrylamide [Other names: acrylamide monomer, 
acrylic amide, propenamide.] This flaky crystal is 
a rather strong toxin used to make polyacrylamide, 
a nontoxic substance used to clear and treat drink- 
ing water, to strengthen paper and for other indus- 
trial uses. It melts at fairly low heat and dissolves 
easily in water; it can be swallowed, inhaled, or 
absorbed through the skin. 

Symptoms 

This neurotoxin affects the skin, eyes, and nervous 
system and can cause severe (sometimes perma- 
nent) brain damage. Symptoms, which may not 
appear immediately, include peeling, reddened 
skin on the hands and feet, a numbness in the 
feet and legs, and sweaty palms and feet. When 
poisoned with acrylamide, the patient may appear 
to be drunk, with an awkward, stumbling gait and 
muted reflexes. 

Treatment 

If there is no vomiting, administer a slurry of acti- 
vated charcoal followed by gastric lavage with saline 
cathartics. Daily doses of vitamins Bi and B12 over 
45 days may protect the central nervous system. 
Pilocarpine may cause a temporary improvement 
in motor activity in some patients, and aspirin or 
phenylbutazone may be given to ease muscle pain. 

Actifed See decongestants. 



adder Any of several poisonous snakes of the 
viper family (Viperidae), plus the death adder, a 



adder, death 3 



viperlike member of the cobra family. (The name 
may also be used for the harmless hognose snake.) 
Adders in the viper family include the common 
adder, the puff adder, and the night adder. No 
adders are found in the United States. 

Although they are related to cobras, adders 
look more like vipers — thick bodies, short tails, 
and broad heads. They range from 18 to 35 inches 
long, with gray or brown skins and dark crosswise 
bands. 

Symptoms 

The symptoms caused by the bite of an adder 
depend in large part on which species makes the 
bite. Some people experience nothing more than 
pain and minor swelling at the bite site; others 
are plagued with chills, fever, falling blood pres- 
sure, convulsions, and bleeding from the gums, 
eyes, and nose. To see symptoms that are specific 
for different species of adders, see the entries 
below. 

Treatment 

Some adder bite victims do not require treat- 
ment; others will die of cardiorespiratory failure 
unless they receive the antivenin. With proper 
treatment, drowsiness and nausea are the worst 
adverse effects, followed by severe bruising and 
swelling at the bite site. For the most effective 
treatment for adder bites, see the individual 
entries below. 

See also adder, common; adder, puff; adder, 

NIGHT. 



adder, common (Vipera berus) This adder is a 
member of the viper family (also called the Euro- 
pean viper) and is the snake that has most com- 
monly made its way into literature. It is found 
throughout Europe and Asia, ranging north of 
the Arctic Circle in Norway, where it survives 
by hibernating through a very long winter. As is 
typical of the more northerly adders, the common 
adder is darker than some of its southern cousins; 
it is usually gray with a black zigzag band on the 
back, with black spots on the side, and its maxi- 
mum length is about 30 inches. Its bite is rarely 
fatal. 



This snake is the only venomous snake in the 
British Isles, where it is regarded with loathing and 
fear, although responsible for very few fatalities. 

Each spring, mating takes place, and ritual fights 
occur between two males, who twist the front part 
of their bodies in a vertical column, each trying to 
push the other over. It is this typical mating behav- 
ior that inspired the two entwined snakes on the 
staff of Hermes the Messenger. This symbol is often 
confused with the staff of Aesculapius, the Roman 
god of medicine, which also features a serpent (the 
Aesculapian snake, a nonpoisonous variety). 

Symptoms 

An immediate sharp pain is followed usually 
within minutes by tingling and local swelhng that 
spreads. Within hours patients experience ten- 
derness, inflammation, spreading pain, enlarged 
lymph nodes, and bruising. The entire hmb may 
become swollen and bruised within 24 hours, and 
in children it can affect the whole body. Some 
people react to a bite with severe anaphylactic 
symptoms within five minutes or up to several 
hours. Hypotension is a very critical sign; symp- 
toms may include nausea, vomiting, diarrhea, uri- 
nary and fecal incontinence, tachycardia, sweating, 
hghtheadedness, shock, hives, bronchospasm, and 
edema of the face, lips, throat, tongue, and gums. 
Bleeding from the nose and gums into the lungs, 
stomach, genitourinary tracts, and other areas 
may occur. Other serious complications include 
coma, seizures, acute renal failure, and acute 
pancreatitis. 

Treatment 

Only a minority of people receive enough venom 
to cause serious complications. Antivenin is avail- 
able and should be given in a hospital setting in 
case the patient has a negative response to the 
antidote. 



adder, death (Acanthophis antarcticus) This 
highly poisonous snake resembles and behaves 
like a viper, although it belongs to the cobra family 
and lives in an area where no vipers are found. It 
can be found in Austraha and New Guinea, has a 
thick body and a broad, flat, triangular head and is 



4 adder, European 



colored gray or brown with dark crossbands. A bite 
from the death adder is fatal about half of the time 
without treatment. Its close relative is the desert 
death adder (Acanthophis pyrrhus), which also has a 
50 percent mortality rate. 

Symptoms 

A bite from a death adder causes paralysis which 
can be minor initially but results in death from 
complete respiratory failure within six hours if 
not treated. Symptoms typically appear within 
15 to 60 minutes and include nausea, vomiting, 
faintness, drowsiness, staggering, slurred speech, 
hemorrhage, and death in about half of untreated 
cases. 

Treatment 

Antivenin is available, but the specific antiserum 
must be given and patients should be tested for 
sensitivity prior to treatment. The antidote is CSL 
death adder antivenin, but it should be given 
only if there is clear evidence that the person was 
poisoned and has been tested for sensitivity. If an 
antivenin is unavailable, anticholinesterases may 
be administered. 

See also cobra; snakes, poisonous. 

adder, European See adder, common. 

adder, night (Causus) A member of the viper fam- 
ily and native to Africa, the night adder is a small, 
thin snake found south of the Sahara. Gray with 
dark blotches, these snakes grow up to a meter 
long and have small fangs and weak venom that 
causes pain and swelhng. There are no recorded 
human fatalities. 

Nocturnally active, this snake spends the day in 
its termite mound or hiding under rocks; it is gen- 
erally slow moving but becomes alert and aggres- 
sive when attacked, inflating its body, flattening its 
neck, and huffing and hissing. 

Symptoms 

The bite of a night adder is extremely painful 
and causes inflammation and occasionally local 
necrosis. 



Treatment 

Antivenin is available and effective against the 
venom, although it generally is not required since 
the venom has relatively low toxicity. However, it 
is always best to treat any bite from a venomous 
snake. 

See also antivenin; snakes, poisonous. 



adder, puff (Bitis) There are several poisonous 
species of puff adder. All members of the viper fam- 
ily, they are found in semiarid savanna and areas 
of rural human habitation in Africa and Arabia. 
This is a sluggish snake that tends to lie still rather 
than flee when approached, but it can strike with 
amazing speed when aroused and is responsible for 
numerous snakebites every year. It gets its name 
from the warning it gives by inflating its body and 
hissing loudly before striking. This extremely poi- 
sonous snake grows from three to five feet long 
and is gray to brown with thin yellow chevrons on 
its back. 

Symptoms 

Seriousness of symptoms depends on the amount 
of venom, if any, injected by the snake. A bite 
typically causes extreme pain and tenderness and 
some necrosis. Serious bites cause the limbs to 
become immovably flexed due to hemorrhaging, 
which typically resolves. Other symptoms may 
include watery blood oozing from the wound, 
nausea, vomiting, blood blisters, hypotension, 
weakness, dizziness, and painful swelling of the 
lymph nodes. If not treated properly, necrosis can 
spread and eventually cause gangrene and loss of 
limbs or digits. Although a puff adder bite is seri- 
ous, less than 10 percent of untreated individuals 
die of a bite. 

Treatment 

Antivenin is available. Death can be avoided if 
adequate antivenin is administered. 

See also adder; adder, common; antivenin; 

SNAKES, POISONOUS. 

Advil (ibuprofen) See anti-inflammatory 
drugs. 



African milk plant 5 



aflatoxins A cancer-causing by-product of the 
Aspergillus flavus mold found in peanuts, corn, wlieat, 
rice, cottonseeds, barley, soybeans, Brazil nuts, and 
pistacfiios. The molds that produce aflatoxin grow 
in warm, humid climates in the southeastern United 
States; the mold can also be produced in the field 
when rain falls on crops, such as com and wheat, that 
are left in the field to dry. Aflatoxin-producing mold 
can even grow on plants damaged by inserts, drought, 
poor nutrition, or unseasonable temperatures. 

Aflatoxin has been called the most potent 
natural carcinogen known to humans; rat studies 
suggest males are more susceptible to cancer fol- 
lowing aflatoxin exposure. Poor diet also seems to 
predispose animals to cancer in the wake of afla- 
toxin ingestion. 

Still, scientists know very little about why or 
how the aflatoxins are produced by the mold, and 
because it is sometimes difficult to see, all sus- 
ceptible crops are subject to routine testing in the 
United States. Unfortunately, it is not possible to 
detect the mold with 1 00 percent accuracy. 

Although the way agricultural products are 
stored can affect the mold's growth, the length 
of time of such storage is also important; the lon- 
ger agricultural products are stored in bins, the 
greater the chance that environmental conditions 
favorable to aflatoxin production will be created. 
Stored nuts or seeds might accidentally get wet, or 
the storage bin might not facilitate drying quickly 
enough to stop the mold from growing. 

Aflatoxins are more common in poor-quality 
cereals and nuts; while most of these low-grade 
products do not enter the human food market, 
they are sold as animal feed, which can go on to 
contaminate animal products (such as meat and 
milk). For this reason, cottonseed meal (a product 
often contaminated with high levels of aflatoxin) is 
banned for use as an animal feed. Cottonseed oil, 
however, rarely contains aflatoxin, since the toxin 
sticks to the hulls of the seed. 

Milk is commonly contaminated with aflatoxin, 
and powdered nonfat milk can contain eight times 
more than the original liquid product, since the 
aflatoxin adheres to the milk's proteins. In addi- 
tion, measurable levels of aflatoxin can be found 
in some baby foods that use dry milk to boost the 
protein content of the product. 



Pasteurization, sterilization and spray-dry pro- 
cessing techniques can substantially reduce afla- 
toxin contamination of dried milk. Meat products 
are less often contaminated because little aflatoxin 
is carried over into the meat, except for pig liver 
and kidneys. Chicken can also become contami- 
nated with aflatoxin when the bird appears to be 
only mildly sick. 

In humans, aflatoxin is believed to cause liver 
cancer, according to some east African studies 
that seem to show a correlation between the two. 
Epidemiological evidence also suggests men are 
more susceptible than women, and many scientists 
believe a poor diet and liver disease also increase 
susceptibility to liver cancer as a result of aflatoxin 
exposure. Data from the African studies were strong 
enough to prompt the Food and Drug Administra- 
tion and the Environmental Protection Agency to 
develop strict regulations to control levels in food 
and animal food sold in the United States. 

Aflatoxin can also cause aflatoxicosis, a condi- 
tion that affects both humans and animals who 
have ingested aflatoxin-contamined food or feed. 
Aflatoxicosis is characterized by abdominal pain, 
vomiting, pulmonary edema, convulsions, coma, 
liver damage, and death. This condition usually 
only occurs in developing countries, and there 
have not been any cases of aflatoxicosis reported in 
humans in the United States. 

Consumers are urged not to eat moldy food, espe- 
cially grains or peanuts, and are urged to be cautious 
about eating unroasted peanuts sold in bulk. 

African milk plant (Euphorbia) There are sev- 
eral species of this poisonous African plant family, 
including E. candelabrum, E. grantii, E. neglecta, E. 
giomgiecpstata, E. systyloides, and E. tirucalli, as well 
as the non-toxic poinsettia. The plants, which are 
reportedly used by African women to eliminate 
troublesome husbands, are found throughout the 
continent. While some of the plants are used for 
medicinal purposes, they are also used as arrow 
poisons (especially the varieties E. candelabrum and 
E. neglecta). While others (notably E. systyloides) are 
used to treat hookworms, too much of the plant 
can cause delirium, convulsions, and death within 
six hours. 



6 Agent Orange 



Poisonous part 

The latex of some species is poisonous, with the 
toxic part being complex terpenes. 

Symptoms 

Irritation of the skin on contact, which may be 
quite corrosive depending on the species. Ingestion 
may cause gastritis. 

Treatment 

For patients experiencing vomiting and stomach 
upset, provide fluids to offset dehydration. 
See also poinsettia. 



Agent Orange See dioxins. 

akee (Blighia sapida) [Other names: ackee, aki, 
arbre, fricasse, vegetal] Named for Captain Bligh, 
captain of the Bounty, this tree produces a fruit that, 
if eaten unripe and unopened, can cause serious 
intoxication and death. The tree grows to 30 or 40 
feet tall with long pairs of leaflets and small, green- 
ish white flowers. A conspicuous red fruit pod splits 
at maturity, with shiny black seeds inside. Native 
to western Africa, akee can be found in the West 
Indies, Florida, and Hawaii. 

Poisonous part 

Although the fruit is perfectly edible when eaten 
ripe and fully opened, the unripe and the rancid, 
spoiled fruit are equally poisonous. Both the fruit 
capsule and its seeds are poisonous, as is the water 
in which the fruit is cooked. 

Symptoms 

Poisoning reaches epic proportions during the 
winter months on the island of Jamaica, where it 
is called "vomiting sickness," and it is often fatal. 
Victims typically experience one of two forms of 
symptoms: vomiting with a remission of eight or 
10 hours followed by more vomiting, convulsions, 
and coma — or convulsion and coma present imme- 
diately. It may take from six hours to a day after 
ingestion for symptoms to appear, although death 
can occur within 24 hours after eating. About 85 
percent of victims experience convulsions. In cases 



of fatal ingestion, hemorrhages can often be found 
in the brain. 

Treatment 

Gastric lavage, fluids, treatment of symptoms and 
intravenous glucose to offset severe hypoglycemia 
(low blood sugar). 

Alar (daminozide) This pesticide has been the 
focus of massive public attention since the 1980s 
in the wake of data suggesting it causes cancer 
and tumors and that it commonly remains as a 
residue on fruits (particularly apples). Assurances 
by growers and the Food and Drug Administra- 
tion that residue levels are very low were suspect, 
since the toxic substance cannot be detected by 
the FDA's routine testing procedures for pesticide 
residues, although specific Alar detection methods 
are available. 

Acceding to public pressure, the manufacturer 
voluntarily withdrew Alar from the market in 
1990. Although Alar is no longer being sold in the 
United States, no restrictions were placed on the 
sale and use of remaining stocks. 

A 1987 study by the Natural Resources Defense 
Council claimed that 38 percent of the U.S. apple 
crop was treated with Alar (especially varieties 
such as Red and Golden Delicious, Mcintosh, Jona- 
than, and Stayman). Residues have not only been 
detected on fresh produce; the residue also appears 
to concentrate in various processed foods, includ- 
ing apple juice, peanut butter, cherry pie filling, 
and Concord grape juice. In 1989, the release of a 
new report by the NRDC pointed out that young 
children are at greater risk from residue than adults 
because they metabolize food differently. 

Although often considered a pesticide. Alar is 
actually a plant growth regulator. It was introduced 
in 1967 for use on apples, peaches, pears, prunes, 
cherries, nectarines, and peanuts. It has also been 
used on cantaloupes, brussels sprouts, tomatoes, 
and grapes. The chemical stops fruit ripening, pre- 
vents fruit from dropping prematurely and allows 
the fruit to develop a deeper, more uniform color. 

Several studies show that Alar causes cancer, 
although the data are not complete; a 1987 study 
by the National Academy of Sciences estimates 



Aldomet 7 



the risk of benign or malignant tumor formation 
associated witfi exposure to Alar to be greater than 
the one in 1 million risk considered acceptable by 
the Environmental Protection Agency. There is 
not enough information to determine whether it 
causes mutations, birth defects, or other problems, 
although evidence suggests it is not a mutagen or 
a teratogen. It is of low toxicity when ingested or 
apphed to the skin. 

aldicarb One of the most toxic pesticides in 
use today, aldicarb has been registered for use 
since 1970. A carbamate insecticide, it is effective 
against a variety of insects, mites, and roundworms. 
Because it is an acutely poisonous pesticide, it is 
not registered for home or garden use, although 
it is registered for use by certified applicators for a 
variety of crops (such as sweet potatoes, peanuts, 
potatoes, oranges, sugar beets, pecans, some seed 
crops, soybeans, and sugarcane). 

Several mass poisoning incidents have been 
reported involving the illegal use of aldicarb on 
unapproved vegetables and fruits; although it is 
not approved for use on watermelons, for example, 
several hundred consumers were poisoned in 1985 
after eating watermelon tainted with aldicarb 
residue. In the long term, exposure to aldicarb has 
been linked with colon cancer. The Agricultural 
Health Study results published in 2007 in the Inter- 
national Journal of Cancer found a 4. 1 -fold increased 
risk of colon cancer associated with exposure to 
aldicarb among pesticide applicators. 

Aldicarb leaches from the soil and has been 
found in groundwater in New York, Florida, Wis- 
consin, Connecticut, Maine, Virginia, Maryland, 
and New Jersey. The problem is especially acute in 
sandy, acidic soils and warm, moist chmates, which 
help move the poison into groundwater. A 2005 
study conducted in the Pacific Northwest, Califor- 
nia, Texas, Southeast, and Mississippi Delta region 
analyzed samples from 1,673 drinking water wells 
that were within 300 meters of fields treated at 
least once between 2002 and 2006 with aldicarb. 
High-performance fiquid chromatography found 
all residues were below the U.S. Environmental 
Protection Agency Health Advisory Limit of 10 
micrograms per liter. 



The manufacturer has specifically prohibited 
the use of aldicarb in areas where drinking water 
has been contaminated. Because it is a systemic 
insecticide, residues of aldicarb probably cannot be 
eliminated by washing produce, although heat in 
cooking may reduce the levels. It is also prohibited 
for use near habitats of endangered bird species, 
because aldicarb is highly toxic to birds, honeybees, 
freshwater fish, and invertebrates. 

Symptoms 

It only takes a very small dose for fatal effects in 
humans. While it is quickly absorbed in the gas- 
trointestinal tract, most is excreted within two 
days after exposure. Tests with rabbits suggest it 
is also readily absorbed through the skin. Symp- 
toms include dizziness, muscle weakness, stomach 
cramping, diarrhea, excessive sweating, nausea, 
vomiting, blurry vision, and convulsions. Although 
studies on long-term exposure are inconclusive, 
there are hints that it may affect the immune sys- 
tem. There is also a potential link to reproductive 
problems. 

Treatment 

Atropine is an antidote for aldicarb poisoning, as it 
is in all carbamate toxicities. 
See also carbamate. 



Aldomet (methyldopa) This is one of a group of 
antihypertensive drugs used to lower blood pres- 
sure. It is available as a white tablet or fiquid. 
Aldomet's effects are strengthened if it is taken 
with other antihypertensives; if taken with alcohol, 
the sedation is deepened and blood pressure faUs 
dangerously low. The effects of a range of other 
drugs are also increased if taken with Aldomet, 
including anticlotting drugs, lithium, or tolbuta- 
mide. Behavior problems may appear if combined 
with Haldol, and blood pressure will soar if com- 
bined with monoamine oxidase (MAO) inhibitors 
or tricycfic antidepressants. 

Symptoms 

Within 20 minutes to an hour after ingestion, 
patients taking an overdose experience drowsi- 
ness, headache, dizziness, weakness, tiredness. 



8 aldrin 



skin rash, joint/muscle pain, impotence, fever, and 
nightmares. 

Treatment 

Atropine or caffeine are used to counteract the 
effects of excessive Aldomet. Activated charcoal 
and cathartic also may be used. Gastric empty- 
ing is not necessary if activated charcoal is given 
promptly. In unresponsive patients, dopamine or 
noradrenaline may be administered. 

aldrin [Other names: Aldrine, compound 118, 
octalene] A component of chlorinated hydrocar- 
bon, aldrin is the most toxic substance used as an 
insecticide dust to control grubs and wireworms 
and as a spray against caterpillars. Used since the 
late 1940s, aldrin is a white, odorless crystalline 
solid that is most poisonous when eaten or inhaled, 
although chronic skin contact can be fatal. A rela- 
tive of DDT, it stimulates the central nervous system 
and is toxic to warm-blooded animals. Along with 
other chlorinated hydrocarbons, aldrin has been 
banned by the Environmental Protection Agency 
since 1974 because of the injurious effects on those 
exposed to it, but European brands are still used for 
termite control. Experimental evidence suggests a 
potential carcinogenic effect. 

Symptoms 

Symptoms begin within one to four hours of expo- 
sure and include headaches, dizziness, nausea, 
vomiting, malaise, convulsions, coma, respiratory 
failure, and death about six hours later. If convul- 
sions begin more than an hour after ingestion, 
recovery is likely. 

Treatment 

The body must be decontaminated, and in cases of 
severe poisoning, an amyl nitrate capsule is given 
under the nose for 1 5 seconds of every minute until 
sodium nitrite and oxygen treatments are started. 
See also chlorinated hydrocarbon pesticides; 

DDT; INSECTICIDES. 

alkaline corrosives The chemical opposites of 
acids, alkalies can be extremely corrosive. The 



most dangerous poisons include sodium hydrox- 
ide, or lye (found in aquarium products, drain 
cleaners and small batteries); potassium hydroxide 
(some small batteries and cuticle remover); sodium 
phosphate (abrasive cleaners); and sodium carbon- 
ate (dye removers and dishwasher soap). Milder 
alkalies (ammonia or bleaches) generally do not 
irreparably burn the esophagus, and the burns 
usually heal without scarring. Mixing alkaline 
corrosives with ammonia, toilet bowl cleaners or 
household cleaners can release hazardous gases 
and is extremely dangerous. 

Inquisitive toddlers in particular are vulnerable 
to injury from alkaline corrosives, which are often 
kept under the sink or in old soda bottles in many 
households. Each year, more than 120,000 Ameri- 
can children under age six ingest such corrosive 
chemicals — mostly household products such as 
detergents and drain openers. 

These extremely corrosive substances can eat 
right through skin. When ingested, they quickly 
burn through internal tissues, injuring the esopha- 
gus; damage can be irreparable for those who 
survive. 

Because of the dangers of ingestion of lye in par- 
ticular, federal legislation has required safety caps 
on containers of more than 2 percent concentra- 
tions of lye. Since then, there has been a decrease 
in the occurrence of these types of poisoning. 

Symptoms 

Alkalies cause an immediate reaction upon contact, 
burning whatever tissues they touch and turn- 
ing the tissue to a fatty liquid. Upon ingestion, 
there is severe pain followed by the inability to 
handle secretions, respiratory problems, collapse, 
and sometimes death. 

Treatment 

Vomiting is never induced in cases of alkali ingestion, 
because it brings up the poison and causes more injury. 
Administration of an antidote in the case of alka- 
line corrosive poisoning is controversial, since by 
the time the person reaches the emergency room, 
it is too late for an antidote. Instead, immediate 
treatment at home should only be at the direction 
of a medical professional or poison control center. 
Once the alkali enters the stomach, it will usually 



amanita mushrooms 9 



be neutralized by gastric acids. All persons who 
ingest alkalies need to be seen as soon as possible in 
a medical facility. The major problem is constricted 
esophagus. 

While the corticosteroid prednisone has 
remained the treatment of choice for the past 30 
years, several studies have questioned its use. 
Recent studies at the Children's National Medical 
Center in Washington, D.C., revealed that those 
treated with prednisone healed as well as those 
who were not. 

In an editorial published in the New England 
Journal of Medicine (September 6, 1991), Frederick 
H. Lovejoy of Children's Hospital in Boston writes: 
"Corrosive injury to the esophagus in children is a 
completely preventable disease." New studies ques- 
tioning the role of prednisone "remove any false 
security derived from believing that an effective 
medical treatment exists." 

If contamination is on the skin or in the 
eyes, wash the area with lukewarm water for 30 
minutes. 

In the ingestion of alkahne disk batteries, there 
have been reports of gastrointestinal bleeding and 
perforation of the esophagus; X-rays are impor- 
tant in these cases. If the battery gets as far as the 
stomach and the person reports no symptoms, no 
further action is required. 

See also ammonia; bleach; lye. 



alkaloids A class of bitter, unpleasant-tasting 
nitrogen-containing compounds including more 
than 5,000 types, ranging from very simple to 
extremely complex. They are found in as many 
as 10 percent of plant species and in a variety of 
animals; the compounds can be isolated for use 
as a drug or poison. Chemically similar to alkahes 
(bases), alkaloids can have strong effects — both 
positive and negative — on the human nervous sys- 
tem, and some affect internal organs as well. 

Some of the most deadly alkaloids include nico- 
tine, taxine, gelsemine and atropine. While most 
alkaloids do occur in closely related plants, a few 
alkaloids are also produced by ladybugs, millipedes, 
ants, toads, and some types of poisonous frogs. 
Researchers at the University of Chicago have 
recently uncovered evidence that suggests that at 



least one variety of bird may also produce alkaloids; 
a yellow and black bird in New Guinea contains the 
chemical batrachotoxin, the same chemical found 
in some types of poisonous frogs. The fingers of 
anyone who handled the bird immediately became 
numb as a result of contact with the alkaloid. While 
there had been no previous evidence of birds con- 
taining a chemical defense system, no one had ever 
looked for such evidence, scientists report. 

Symptoms 

When ingested, most alkaloids produce a very 
strong physiological reaction, usually acting on 
the nervous system in ways that are still little 
understood. 

Treatment 

Potassium permanganate. 

See also atropine; gelsemine; nicotine; taxine. 

amanita mushrooms Of the Amanita genus of 
about 100 mushrooms of the family Amanitaceae, 
between 25 and 35 are found in the United States. 
Some of the amanitas are extremely poisonous and 
include the false morel, fly agaric, panther mush- 
room and — most deadly of all — the destroying 
angel or death cap (Amanita phalloides). Mycologists 
disagree about the classification of many of the 
closely related amanita mushrooms, however, and 
other sources may differ in these classifications. 

Most of the cases of mushroom poisoning in 
the United States can be traced to the amanitas, 
particularly A. muscaria and A. phalloides, which are 
also sometimes referred to as toadstools (from the 
German word for "death"). They have been known 
to be poisonous since ancient times. 

Particularly dangerous are the snow-white to 
pale green or tan amanitas. The amanitas typi- 
cally have white spores, a ring on the stem slightly 
below the cap, a veil that is torn as the cap expands 
and a cup from which the stalk arises. 

Poisonous part 

There are two types of toxic compounds in the ama- 
nitas, which cause two separate syndromes in those 
who consume them. In A. phalloides, the substance 
amanitine is responsible for the major symptoms; 



10 amatoxins 



phalloidine produces degenerative changes in the 
kidney, liver, and heart muscles. Cooking the 
deadly Amanita does not destroy their toxicity, and 
it is estimated that just one A. phalloides cap can 
kill an adult. Amanitas that feature amatoxins and 
phallotoxins include A. phalloides, A. verna, A. virosa, 
A. bisporigera, A. ocreata, A. suballiacae, and A. tenuifo- 
lia. Amanitas that contain the toxins muscimol and 
ibotenic acid include A. muscaria, A. pantherina, A. 
gemmata, A, cokeri, and A. cothurnata. 

Symptoms 

In A. muscaria, rapid poisoning occurs from a few 
minutes to two hours after ingestion, depending 
on the amount of toxin present; symptoms include 
salivation, sweating, cramps, diarrhea, vomiting, 
circulatory failure, mental disturbances, coma, 
and convulsions. Death is rare from A. muscaria 
poisoning. A more deadly poisoning occurs from 
A. phalloides, whose symptoms never appear before 
six hours after ingestion. When they do appear, 
they include the sudden onset of colicky abdomi- 
nal pain, vomiting, and severe diarrhea that may 
contain blood and mucus. This type of diarrhea is 
so severe that it is very similar to the symptoms of 
cholera. Even without treatment, the victim may 
appear to begin recovering but two to four days 
after ingestion will experience liver, heart, and 
kidney damage, circulatory failure, convulsions, 
coma, and death. 

Treatment 

Many antidotes to Amanita poisoning have been 
reported, but most of this information has been 
anecdotal. Some victims of severe Amanita poison- 
ing have been treated successfully with a combi- 
nation of thioctic acid, glucose, and penicillin, or 
by filtering the blood through charcoal. Gastric 
lavage is indicated, if the patient has not vomited 
already, followed by activated charcoal and saline 
cathartics. 

See also amatoxins; destroying angel; fly 

AGARIC; MUSHROOM POISONING; MUSHROOM TOXINS; 
PANTHER MUSHROOM. 



amatoxins A group of very toxic peptides found 
in a few species of poisonous mushrooms, includ- 



ing Amanita phalloides, A. virosa, A. ocreata, A. verna, 
Galerina autumnalis, G. marginata and a few types of 
Lepiota. Amatoxins are among the strongest toxins 
in the world; the lethal dose is just 0.1 milligram 
per kilogram, but one amanita mushroom cap may 
contain between 10 and 15 milligrams of toxin. 

The Meixner test may detect the presence of 
amatoxins in mushrooms; their presence is indi- 
cated by a blue color that appears after one drop 
of concentrated hydrochloric acid is added to 
dried juice from the mushroom cap dripped onto 
unrefined paper. However, this test should not 
be used to determine whether it is safe to eat a 
mushroom. 

See also Amanita mushrooms; mushroom poi- 
soning; MUSHROOM toxins. 

americium In 1944, four American scientists 
produced a radioactive rare earth metal called 
americium by bombarding plutonium-239 with 
high-energy neutrons. The plutonium-240 changed 
into plutonium-241, which then decayed into 
americium-241, which consists mainly of man- 
made radioactive isotopes. 

Americium can be produced in large quantities, 
but the element has few practical uses. Because 
it is radioactive it must be handled with caution. 
Generally, it is used in smoke detectors and medi- 
cal diagnostic devices, to help make flat glass, and 
as a portable source of gamma rays in radiography. 
However, it is extremely expensive to produce in 
usable quantities. 

Humans are typically exposed to high concen- 
trations of americium through food, breathing, 
or skin contact associated with the release of the 
metal during nuclear production and accidents, or 
by working in or living near nuclear power plants. 
Low levels of americium may be present in water 
and soil because of atmospheric nuclear weapons 
testing prior to the nuclear test ban of 1963, as the 
element can remain in the atmosphere for decades 
and travel around the globe, setthng to earth over 
time. Because the isotopes decay very slowly in the 
environment, they have the potential to damage 
animals that are exposed to high levels. Americium 
that enters the soil may end up in plants, but typi- 
cally only in very small, nontoxic amounts. 



amphetamines 11 



Symptoms 

Once americium is in the body, it can become con- 
centrated in the bones, where it will remain for a 
long time and slowly decay, releasing radioactive 
rays and particles. The rays can alter genetic mate- 
rials and cause bone cancers. Damage to organs is 
very unlikely, however, because americium does 
not remain in organs for long. 

Treatment 

Oral dose of a simple aqueous solution of zinc- 
diethylenetriaminepenta-acetic acid (DTPA) is 
effective in treatment of poisoning with pure 
americium. 



ammonia This colorless, strong-smelhng poison 
gas is formed by blowing steam through incandes- 
cent coke. Extremely toxic when inhaled in con- 
centrated vapors, ammonia is irritating to both eyes 
and mucous membranes. It is one of the top five 
most common inorganic chemicals produced in 
the United States, where it is used in refrigerants, 
and to manufacture detergents, permanent wave 
lotions and hair bleaches, and cleaning agents. 
It is also used in the manufacture of explosives 
and synthetic fabrics, herbicides, fertihzers, and 
pesticides. 

Ammonia has been shown to produce skin 
cancer in humans in doses of 1,000 milhgrams per 
kilogram of body weight. It also irritates the lungs 
and can cause swelling of lung tissue. It may even 
cause explosions if mixed with silver or mercury. 

Ammonium hydroxide (ammonia water) is a 
weak alkali formed when ammonia dissolves in 
water. This clear, colorless liquid contains between 
10 and 35 percent ammonia and is used as an 
alkali in metallic hair dyes, hair straighteners, and 
protective skin creams; it is also used in detergents, 
stain removers, and ceramics. 

Symptoms 

Ammonia fumes can irritate the eyes and upper 
respiratory tract, causing vomiting, conjunctivitis 
and inflammation of the lips, mouth, and throat. 
Toxic cases of inhalations cause airway obstruction, 
pulmonary irritation with swelling, cyanosis, bron- 
chitis, and pneumonia. Ammonia can damage cells 



directly, and skin contact can lead to dermatitis; 
ingestion can burn the esophagus. 

Treatment 

The ammonia is diluted or neutralized with water 
or milk, but the victim should not vomit, as the 
substance could burn the mouth or throat, espe- 
cially in concentrations greater than 5 percent. For 
eye contamination, wash the eyes with running 
water for 1 5 to 20 minutes. If ammonia is inhaled, 
move the victim to fresh air and give artificial 
respiration. 

amnesic shellfish poisoning (ASP) This type of 
shellfish poisoning was first identified in Canada 
in a 1987 outbreak that killed three and sickened 
more than 100 people, leading to significant mem- 
ory loss and confusion. ASP is associated primarily 
with mussels. The poisoning is especially serious 
with older patients and may appear to resemble 
Alzheimer's disease. All known fatalities have 
occurred in elderly patients. 

Symptoms 

Initial symptoms appear within 24 hours, and 
neurological symptoms follow within 48 hours. 
ASP can be life threatening, causing stomach prob- 
lems (vomiting, diarrhea, and abdominal pain). In 
severe cases, neurological problems (confusion, 
memory loss, disorientation, seizure, and coma) 
also appear. 

Prevention 

Eat only shellfish from reportable sources and 
approved beds. 

amphetamines [Other names: beans, bennies, black 
beauties, black mollies, copilots, crank, crossroads, 
crystal, dexies, doublecross, hearts, meth, miniben- 
nies, pep pills, roses, speed, thrusters, truck drivers, 
uppers, wake-ups, whites. Trade names: Aktedron, 
Benzedrine, Elastonon, Orthedrine, Phenamine, 
Phenedrine.] This white powder (or colorless 
liquid) is a highly addictive stimulant, once widely 
prescribed as a diet pill — but this use has now been 
banned by the Food and Drug Administration. 



12 amyl nitrite 



Amphetamines were also used to treat Parkin- 
son's disease and similar symptoms, depression, 
alcohol withdrawal, premenstrual tension, and 
hyperactivity. Today, they are strictly controlled 
and seldom administered because of serious with- 
drawal problems and dangerous side effects. 

Usually taken in pill form, amphetamines can 
also be injected when in solution. 

(A form of amphetamine commonly known as 
"speed" or "meth" — methamphetamine — is usually 
injected intravenously, although speed also comes 
in oral doses.) 

Symptoms 

Amphetamines can stimulate both the sympathetic 
and central nervous systems, and are toxic in levels 
only slightly above usual doses, although a degree of 
tolerance can develop over time. Symptoms appear 
within 30 minutes to an hour, and when these drugs 
are taken in too large a dose, the symptoms can 
include sleeplessness, restlessness, tremors, palpita- 
tions, nausea, vomiting, diarrhea, anorexia, delirium, 
hallucinations, euphoria, nervousness, confusion, 
irritability, short temper, depression, cyanosis, sweat- 
ing, convulsions, coma, and cerebral hemorrhages. 
Brain damage or death may result from ventricular 
arrhythmia or stroke. When amphetamines are 
taken in only a mild overdose, symptoms include 
fatigue, mental depression, and high blood pressure. 
Those who chronically abuse amphetamines may 
develop heart problems and behavioral abnormali- 
ties (such as picking at the skin) and appear paranoid 
and anorexic. In fact, appetite suppression in long- 
term addicts can continue for up to two months after 
amphetamine use has stopped. 

Treatment 

Isolate the victim in a quiet, darkened room to avoid 
overstimulation and possible heart failure. Gastric 
lavage may be helpful if the person is awake, but 
emesis is not induced because of the risk of abrupt 
onset of seizures. Administer activated charcoal 
and a cathartic. Other symptoms are treated, and 
Valium may be given to slow the heartbeat. 

amyl nitrite An antispasmodic, this is an antidote 
of cyanide and ergot that is also used medically to 



dilate the coronary vessels and lower blood pres- 
sure. It has been used as a vasodilator in angina 
therapy for a long time and has also been used as an 
industrial chemical and perfume scent. The increas- 
ing abuse of amyl nitrite "poppers" led to their 
restriction and the increased popularity of butyl 
and isobutyl nitrites (related volatile compounds 
sold over the counter as room odorizers under such 
names as "Locker Room"). These are inhaled to 
produce highs and intensify sexual orgasms and are 
sometimes sprayed in discos to stimulate dancing. 

Symptoms 

Inhaling the volatile nitrites dilates blood vessels, 
causing low blood pressure lasting about 90 sec- 
onds. Other symptoms include pulsating headache, 
rapid flushing of the face, dizziness, confusion, 
vertigo, restlessness, weakness, blue skin, nausea, 
and vomiting. In addition, butyl nitrite sniffing 
has caused mild methemoglobinemia in otherwise 
healthy patients. Chronic abuse of amyl nitrite can 
cause anemia. 

Treatment 

Administration of methylene blue may be effective 
in treating methemoglobinemia. Other treatment 
is symptomatic. 

Anaprox See nonsteroidal anti-inflammatory 

DRUGS. 



anectine (succinylcholine) This extremely fast- 
acting drug is also known as curare and is one of a 
group of neuromuscular blocking agents that affects 
skeletal muscles. It is used to promote muscle relax- 
ation during surgical anesthesia and is sometimes 
given to control convulsions. It is generally used 
in the operating room during lung procedures, as 
it stops normal breathing and allows the patient 
to be placed on a respirator. Many physicians also 
use it before surgery as a muscle relaxant because 
it cuts down on the amount of anesthesia needed. 
It is also an antidote for strychnine poisoning and 
an anticonvulsant treatment for tetanus (lockjaw). 
An effective dose can be fatal if breathing is not 
maintained artificially. This bitter, white powder 



anesthetics, local 13 



dissolves easily in water and can be administered 
either in the muscle or in the veins. 

Symptoms 

Almost immediately upon injection, anectine pro- 
duces respiratory paralysis by blocking the neuro- 
muscular transmissions. Symptoms will continue 
for one to 10 minutes after the injection is dis- 
continued. Cardiac arrest has occurred during the 
administration of anectine after a head injury. 

Treatment 

There is no antidote — anectine works too quickly. 
See also curare; neuromuscular blocking 

AGENTS. 



anemone, sea One of the most abundant of the 
coelenterates, these immobile flowerhke creatures 
range in size from a few milhmeters to about one 
and a half feet with long tentacles. Anemones are 
tube-shaped animals usually fixed to a firm surface, 
with a mouth slit on top and a range of tentacles 
around the mouth. 

There are thousands of varieties of anemones, 
which differ from one another in every way. They 
do share one trait in common, however: the ability 
to sting and paralyze a victim with specialized cells 
lining their tentacles, which — while not usually 
fatal in itself — can cause drowning. Some varieties 
are poisonous to eat as well as capable of delivering 
a venomous sting. 

While not all sea anemones are poisonous, the 
Matamalu samasama from Samoa (Radianthus pau- 
motensis, Rhodactis howesii) is poisonous when eaten 
raw or cooked and causes respiratory failure. The 
Actinia equina floats along the eastern Atlantic, in 
the Mediterranean Sea, the Black Sea, and the Sea 
of Azov; the hell's fire sea anemone (Actinodendron 
plumosum) is found in tropical waters of the Pacific 
Ocean and the Great Barrier Reef off Australia; and 
the rosy anemone (Sagarita elegans) inhabits the 
waters off Iceland to the Mediterranean Sea and 
the coast of Africa. 

Symptoms 

Effects of the sea anemone sting are usually local, 
causing itching, burning, swelling, and reddening 



followed by sloughing of the skin. The tissues may 
then slough off followed by a long period of puru- 
lent discharge, and multiple abscesses may occur. 
More generalized symptoms include fever, chills, 
abdominal pain, nausea, vomiting, diarrhea, head- 
ache, thirst, and prostration. 

Treatment 

Soak the stung area in water as hot as possible 
without scalding the person for up to one hour, 
using hot soaks while on the way to the doctor. 
Observe for signs of shock. The ulcers resulting 
from a sea anemone sting are usually slow to heal 
and can be resistant to treatment. Baking soda in a 
paste with water should be apphed to the sting to 
relieve pain. Calamine lotion will also help ease the 
burning sensation, and painkillers may help with 
the stinging pain. (Other local remedies for pain 
used around the world include meat tenderizer, 
sugar, ammonia, and lemon juice.) 

anesthetics, gaseous/volatile These drugs include 
ether, chloroform, ethylene, and cyclopropane. 
They are also found as gases, including ethylene, 
cyclopropane, and nitrous oxide. 

All these anesthetics produce general anesthe- 
sia; at cold temperatures, they are volatile hquids 
before they become gases and can be inhaled or 
ingested. 

Symptoms 

Overdose stops respiration and interferes with the 
action of the autoimmune system, causing uncon- 
sciousness, respiratory failure, cyanosis, and heart 
irregularities. 

Treatment 

Remove gas, maintain respiration, and keep warm. 
In the event of fever, lower temperature with wet 
towels. 

See also chloroform; cyclopropane; ether. 

anesthetics, local These drugs are used to numb 
one particular area of the body either by injection 
or by topical skin application (and include epidu- 
ral, spinal, and regional nerve blocks). No two act 



14 aniline 



the same, and their effect on patients varies from 
one person to another depending on the person's 
physical makeup. These drugs are all related to 
cocaine and are synthetic versions of the coca 
bush alkaloids. Local anesthetics include procaine, 
lidocaine, marcaine, monocaine, nesacaine, nup- 
ercaine, duranest, xylocaine, carocaine, oracaine, 
unacaine, citanest, and novocaine. Of these, pro- 
caine is considered the most dangerous and has 
caused numerous fatalities; shock can occur with 
only very small doses, and it enhances the action 
of muscle relaxants. 

All of the local anesthetics are colorless (either 
liquid or gel) and are injected. 

Symptoms 

Local anesthetics work by blocking the nerve sig- 
nals, providing a local loss of sensation. When the 
drugs are given in overdose, these actions may 
cause central nervous system and cardiovascular 
toxicity. Toxic levels can result from a single exces- 
sive injection, from a series of smaller injections or 
by accumulation of drug level by repeated doses. 
Symptoms of systemic poisoning affect primarily 
the central nervous system and include giddiness, 
feelings of oppression, severe collapse, coma, con- 
vulsions, dizziness, cyanosis, low blood pressure, 
tremors, coma, irregular and weak breathing, 
bronchial spasm, and heart failure. Repeated skin 
apphcations of local anesthetic can cause hyper- 
sensitivity, including itching, redness, swelling, and 
blistering. 

Treatment 

First, the injected drug must be removed from 
the body and absorption from the injection site 
lessened by using a tourniquet or ice pack. Treat 
symptoms, maintain airway and give artificial res- 
piration with oxygen to control convulsions and 
central nervous system depression. 
See also lidocaine; procaine. 

aniline (amino benzol) A colorless, oily fluid that 
turns brown when exposed to air, used in inks for 
stamp pads, printing, and cloth marking, in addition 
to dyes, paint removers, and paint. Aniline can be 
ingested or absorbed as a gas, powder, or liquid. 



Occasionally, anihne dye poisonings do occur 
among infants and young children; newborns have 
been poisoned by touching — and inhaling fumes 
from — diapers freshly stamped with anihne dye. It 
is also possible to become poisoned from absorbing 
shoe polish that contains aniline dyes. Fortunately, 
there are few poisonings from this substance 
today. 

Symptoms 

Aniline interferes with the transportation of oxygen 
throughout the central nervous system, and within 
two hours after exposure, moderate exposure may 
cause cyanosis of the lips, ears, and cheeks. In more 
severe cases, symptoms of cyanosis are much more 
marked, together with headaches, shallow breath- 
ing, vertigo, chills, nausea, and vomiting. Infants 
are apathetic and may exhibit convulsions, coma, 
and death. Direct contact of aniline dye with the 
skin will cause dermatitis. Chronic poisoning in the 
wake of inhalation or skin absorption causes mild 
cyanosis, anorexia, weight loss, weakness, head- 
ache, vertigo, irritability, and anemia. 

Treatment 

Remove victim to fresh air. If the skin has been con- 
taminated, wash thoroughly with vinegar followed 
by soap and water. If aniline has been ingested, 
administer gastric lavage followed by hquid petro- 
latum and a sahne cathartic. Oxygen, doxapram, 
and blood transfusions may also be necessary. In 
very severe cases, hemodialysis should be used. 

Animal Poison Control Center A 24-hour emer- 
gency center staffed by veterinary health pro- 
fessionals trained to handle pet poisonings. Pet 
owners who can't reach a vet or other local experts 
can call this center by dialing (888) 426-4435. A 
$60 consultation charge may be applied to your 
credit card. 

The nonprofit organization, affiliated with the 
college of veterinary medicine of the University of 
Illinois, is an operating division of the American 
Society for the Prevention of Cruelty to Animals. It 
was begun in 1978 and began charging for its ser- 
vices in 1990. All employees are veterinarians with 
clinical experience, with additional six months' 



Antabuse 15 



training in toxicology; two are board certified with 
the American Board of Veterinary Toxicologists. In 
addition, the animal poison control center supports 
a backup laboratory to provide additional toxico- 
logical assistance. 

The center fields calls equally from private 
pet owners and veterinarians and maintains an 
extensive log of poisoning cases from more than 
4,000 different toxic agents. The kinds of animal 
poisoning cases vary according to the time of 
year: pesticides and flea and tick poisonings in 
the summer; chocolate and poinsettia poisonings 
during the Easter and Christmas holidays. Most 
calls are due to poisoning from insecticides used 
in and around the house or on the farm. The 
center handles problems with livestock as well 
as household pets, from dogs and cats to canaries 
and potbelly pigs. 

Poisonings with human medications make up as 
many as 20 percent of the calls to the animal poi- 
son center, especially heart pills and birth control 
pills left on nightstands. Toxic plants are a third 
major category. 

anisakiasis A disease of the intestines caused by a 
parasitic worm Anisakis simplex, which infests small 
crustaceans eaten by many kinds of fish, dolphins, 
and whales. Humans become infected by eating 
improperly prepared fish. 

Fewer than 10 cases are diagnosed in the United 
States every year; however, experts suspect many 
cases go undiagnosed. Japan has the greatest num- 
ber of cases because of the large amounts of raw 
fish the Japanese eat, but it also occurs in Scandi- 
navia and Latin America. Anisikiasis is easily mis- 
diagnosed as acute appendicitis, Crohn's disease, 
gastric ulcer, or gastrointestinal cancer. 

The larvae are found in raw, undercooked, or 
insufficiently frozen fish and shellfish, and its inci- 
dence is expected to increase with the increasing 
popularity of sushi and sashimi bars. Cod, had- 
dock, fluke, flounder, and monkfish have also been 
known to host the parasite. 

Symptoms 

Symptoms usually begin within six hours after 
consuming raw or undercooked seafood. If the lar- 



vae is not coughed up or passed into the bowels, it 
can penetrate the stomach and cause severe pain, 
nausea, and vomiting. In severe cases, the pain is 
akin to acute appendicitis. 

Diagnosis 

In North America, the infestation is usually diag- 
nosed when the patient begins to feel a tingling 
or tickling sensation in the throat and coughs up 
a worm. Alternatively, a physician may need to 
examine the inside of the person's stomach and the 
small intestines. 

Treatment 

Surgically removing the worm(s) may be neces- 
sary. Most patients recover without treatment. 

Prevention 

The worm is killed by cooking or freezing the fish. 
Marinating raw fish in lemon or vinegar does not 
kill all the harmful bacteria or parasites that the 
fish might contain. Sushi lovers should eat only 
at reputable restaurants and ask whether the fish 
was previously frozen (freezing reduces the risk 
of illness by killing larvae of parasites that might 
have been present in the raw fish). The larval stage 
of the worms are killed by cooking at 140°F for at 
least 10 minutes. 



Antabuse (disulfiram) This drug is used to treat 
alcoholics, who experience an extremely unpleas- 
ant side effect if they drink alcohol while taking 
it. Long-term use of Antabuse can damage the 
peripheral nerves. 

Symptoms 

An acute overdose may cause vomiting, clumsiness, 
lethargy, seizures, and coma. Several deaths have 
been reported as a result of liver failure. Ingestion 
of alcohol (including some types of cough syrup 
or other alcohol-containing products) while taking 
Antabuse can cause flushing, throbbing headache, 
anxiety, vertigo, vomiting, and convulsion; the 
severity of the reaction is tied to the amount of 
Antabuse and alcohol ingested. It generally takes 
at least one day on the drug before the interaction 
will set off this reaction, but the reaction will also 



16 Anthrax 



occur up to several days after tfie last dose of Anta- 
buse fias been talien. 

Treatment 

There is no specific antidote. For overdose of Anta- 
buse: Induce vomiting or perform gastric lavage; 
administer activated charcoal and a cathartic. For 
interaction of Antabuse and alcohol: once symp- 
toms appear, there is not much that can be done; if 
the victim drank a large amount of alcohol, gastric 
lavage and activated charcoal should help. 

Anthrax See Bacillus anthracis. 



antianxiety drugs A group of drugs used to relieve 
symptoms of anxiety; benzodiazepines and beta 
adrenergic blockers are fast acting and used to be 
the main drugs prescribed for anxiety, although 
most are addictive. Among them are Xanax (alpra- 
zolam), Librium (chlordiazepoxide), Tranxene 
(chlorazepate), Valium (diazepam), Dalmane (flu- 
razepam), Ativan (lorazepam), Serax (oxazepam), 
Centrax (prazepam), and Halcion (triazolam). How- 
ever, benzodiazepines have been largely replaced 
by selective serotonin reuptake inhibitors (SSRIs). 
Among the preferred SSRIs for generalized anxiety 
disorder are Paxil (paroxetine), Lexapro (escitalo- 
pram), and Effexor (venlafaxine). Prozac (fluox- 
etine) and Zoloft (sertraline) are also prescribed. 

Symptoms 

Overdose of benzodiazepines and beta adrenergic 
blockers can bring on drowsiness, weakness, dou- 
ble vision, clumsiness, lethargy, convulsions, coma, 
cyanosis, and breathing problems. Chronic abuse 
can cause skin rash, gastric upset, headaches, and 
blurred vision. Overdose of SSRIs may cause sero- 
tonin syndrome, which is characterized by restless- 
ness, hallucinations, shivering, nausea, diarrhea, 
headache, tremor, agitation, and diaphoresis. Most 
reports of fatalities with antianxiety drugs involve 
multiple drug ingestions. 

Treatment 

For benzodiazepines and beta adrenergic blockers, 
induce vomiting or perform gastric lavage followed 



by the administration of activated charcoal and a 
saline cathartic. Follow with supportive measures, 
including monitoring of blood pressure and fluid 
levels. For SSRIs, gastric lavage is generally not 
indicated unless it can be performed within one 
hour of the overdose and provided the airway 
is secure. Airway compromise is highly possible 
because of deterioration of mental status and neu- 
romuscular dysfunction. Use of activated charcoal 
should be administered with careful attention to 
the possibility of such compromise. 

See also benzodiazepines; beta adrenergic 
BLOCKERS; Dalmane; selective serotonin reuptake 

INHIBITORS. 



antiarrhythmic drugs Prescribed to control 
unwanted or abnormal heart rhythms. The Ameri- 
can Heart Association lists four main categories of 
drugs used to treat arrhythmias: 

1. beta-adrenergic blockers (e.g., atenolol [Tenor- 
min], carvedilol [Coreq], propranolol [Inderal]) 

2. calcium channel blockers (e.g., diltiazem [Cardi- 
zem], verapamil [Calan]) 

3. sodium channel blockers (e.g., quinidine, pro- 
cainamide [Pronestyl], disopyramide [Norpace]) 

4. potassium channel blockers (e.g., amiodarone 
[Cordarone], bepridil [Vascor]) 

5. miscellaneous (e.g., digoxin [Lanoxin], adenos- 
ine [Adenocard]). All of these drugs may be 
toxic and even fatal in doses only slightly above 
the recommended dose, and for some people 
they are toxic even within the therapeutic 
range. 

Symptoms 

Toxicity with antiarrhythmic drugs primarily affects 
the cardiovascular and central nervous systems. 
Symptoms include heartbeat irregularities, dry 
mouth, dilated pupils, dehrium, seizures, coma, 
and respiratory arrest. Quinidine often causes nau- 
sea, vomiting, diarrhea, and, with chronic doses, 
cinchonism (ringing in the ears, vertigo, deafness, 
and visual disturbances). Procainamide may cause 
upset stomach and a lupus-like syndrome with 
chronic use. 



antidepressants 17 



Treatment 

Heart problems are treated with hypertonic sodium 
bicarbonate and possibly insertion of a pacemaker; 
treat symptoms and monitor vital signs. Do not 
induce vomiting because of the risk of rapid onset 
of seizures; perform gastric lavage followed by acti- 
vated charcoal and a cathartic. 

See also beta adrenergic blockers; digitalis; 

QUINIDINE. 



anticoagulants Drugs used to keep the blood 
from clotting too quickly and reduce mortal- 
ity associated with blood clots. They include 
(1) warfarin, dicumarol, phenprocoumon, and 
phenindione, which work by interfering with the 
production in the liver of various clotting factors 
that depend on vitamin K; and (2) argatroban, 
bivalirudin, and lepirudin, newer drugs that 
inhibit thrombin (clot factors). Warfarin sodium 
(Coumadin) is the least toxic, and most widely 
used, anticoagulant. A wide range of factors can 
influence a person's response to anticoagulants, 
including changes in diet, environment, and 
medication. 

Symptoms 

Sudden rush of blood hemorrhaging of the larynx, 
trachea or lungs, bloody stools, hermorrhages 
in other organs, bruising and bleeding into joint 
spaces, skin rash, vomiting, fever, and kidney 
damage. Repeated use leads to acute poisoning. 
Fatalities from kidney and liver damage have been 
reported after repeated doses, and death may not 
occur until several weeks after the drug has been 
discontinued. 

Treatment 

Complete bed rest; medication is administered to 
prevent internal bleeding. 
See also warfarin. 



antidepressants A class of drugs used to treat 
depression and anxiety. There are several different 
kinds of antidepressants that are grouped according 
to which chemicals in the brain they affect. Selec- 
tive serotonin reuptake inhibitors (SSRIs) tend to 



have fewer side effects than other antidepressants. 
The SSRIs include citalopram (Celexa), escitalo- 
pram (Lexapro), fluoxetine (Prozac), paroxetine 
(Paxil), and sertraline (Zoloft). These are typically 
the first choice for treatment of depression. Combi- 
nation drugs are also high on the list of treatment 
options and include serotonin and norepinephrine 
reuptake inhibitors (duloxetine [Cymbalta] and 
venlafaxine [Effexor]), one norepinephrine and 
dopamine reuptake inhibitor (bupropion [Well- 
butrin]), and a combination of reuptake inhibi- 
tor and receptor blocker (mirtazpine [Remeron] 
and trazodone [Desyrel]). The second line of 
treatment is tricyclic antidepressants (now more 
accurately called cyclics, or CAs), which include 
amitriptyline (Elavil), desipramine (Norpramin), 
imipramine (Tofranil), maprotiline (Ludiomil), and 
nortriptyline (Aventyl). The least commonly used 
antidepressants are the monamine oxidase inhibi- 
tors (MAOIs), which include isocarboxazid (Mar- 
plan), phenelzine (Nardil), and tranylcypromine 
(Parnate). 

Symptoms 

An SSRI overdose infrequently results in the 
development of serotonin syndrome (characterized 
by restlessness, hallucinations, shivering, nausea, 
diarrhea, headache, tremor, agitation, and diapho- 
resis), but other patients who remain asymptom- 
atic for several hours after overdosing usually do 
not need medical treatment. Research shows that 
individuals who take up to 30 times the daily dose 
of an SSRI typically have few or no side effects. 
Overdose of cyclic antidepressants, however, can 
be very serious, and is associated with central ner- 
vous system symptoms, including hallucinations, 
confusion, and lethargy that progresses to seizures 
or coma. Their most serious effect is on cardiac 
conductivity, resulting in multiple heart arrhyth- 
mias, which may result in death. Acute overdose of 
MAO inhibitors causes slow heartbeat, confusion, 
hallucinations, agitation, and convulsions. High 
blood pressure may quickly reverse to low blood 
pressure, which is an indication of a very seri- 
ous prognosis. Beer, wine, and cheese eaten with 
MAO inhibitors can cause very serious symptoms, 
including intracranial bleeding, circulatory failure, 
and death. 



18 antifreeze 



Treatment 

The victim should be under medical supervision, 
since induced vomiting could cause seizures or 
arrhythmias. At a hospital, gastric lavage is fol- 
lowed by administration of activated charcoal and a 
cathartic. For cases of severe overdose of CA, phy- 
sostigmine sahcylate may be used as an antidote. 
Hospitalization is strongly recommended. Patients 
receiving good supportive care will recover within 
four days. 

See also monoamine oxidase (mao) inhibitors. 

antifreeze Most types of antifreeze contain ethyl- 
ene glycol or methanol, both of which are poison- 
ous to drink. About 50 deaths occur each year in 
the United States from antifreeze poisoning, most of 
which are among alcoholics who turn to antifreeze 
as an alternative to alcohol; some people attempt 
to commit suicide by this method. Antifreeze poi- 
soning is also a problem for household pets, who 
are attracted by the sweet taste. According to Dr. 
Steve Hansen of the National Animal Poison Con- 
trol Center, it only takes one teaspoon of undiluted 
antifreeze/coolant to kill a seven-pound cat. 

Poisonous part 

Antifreeze containing ethylene glycol is extremely 
toxic because of its breakdown products and result- 
ing acidosis. 

Symptoms 

In small amounts, antifreeze poisoning resembles 
intoxication from alcohol; large doses cause vom- 
iting, seizures, and coma within a few hours, 
followed by acute kidney failure within 24 to 36 
hours. The lethal dose of ethylene glycol is con- 
sidered to be 100 milhliters for an adult, although 
recovery has been noted after ingestions ranging 
up to 970 milhliters. Antifreeze containing metha- 
nol can also cause blindness. 

Treatment 

The victim should be taken to a medical care 
facihty immediately. Fomepizole is used to treat 
antifreeze poisoning. If the eyes are contaminated, 
immediately rinse with warm running water for 1 5 
to 20 minutes. 



For antifreeze poisoning in pets, owners should 
first feed the pet soft food (milk or canned pet food) 
and then induce vomiting using syrup of ipecac. 
Fomepizole also may be used for pets. // the pet is 
found within one hour of poisoning, alcohol (such as 
whiskey) may be given as an antidote after vomit- 
ing — one or two ounces for smaller dogs and up to 
three or four ounces for larger breeds. If more than 
five hours have elapsed since poisoning, emergency 
home treatment will be fruitless. Animal ingestion of 
antifreeze is a serious emergency that requires immediate, 
intensive veterinary care. Vomiting and alcohol should he 
administered at home only when veterinary care is not 
immediately available. For advice in an animal poi- 
soning emergency, call the National Animal Poison 
Control Center at (888) 426-4435 ($60 per call). 
The center's phones are staffed by trained veteri- 
narians 24 hours a day, seven days a week. 

See also fomepizole; methyl alcohol; Animal 
poison control center. 



antihistamines A group of drugs that block the 
effects of histamine, a chemical released during 
an allergic reaction. While harmless in normal 
amounts, they can be fatal when taken in mas- 
sive overdose (as in a suicide attempt or accidental 
ingestion by young children). Antihistamines are 
being used more and more, not only to treat aller- 
gies and respiratory infections but also for motion 
sickness and as sedatives. Many are available over 
the counter. 

Examples of over-the-counter (OTC) antihis- 
tamines include brompheniramine (Dimetapp, 
Nasahist), chlorpheniramine (Chlor-Trimeton), 
clemastine (AUerhist, Tavist), and diphenhydramine 
(Benadryl), all of which belong to the first genera- 
tion of antihistamines. Common second-generation 
antihistamines include loratadine (Claritin, OTC) 
plus prescriptions cetirizine (Zyrtec), desloratadine 
(Clarinex), and fexofenadine (Allegra). Second- 
generation antihistamines are much less likely to 
cause drowsiness and dry mouth than are first- 
generation drugs. 

Symptoms 

Antihistamines are a central nervous system 
depressant, causing drowsiness, dizziness, and 



anti-inflammatory drugs 19 



clumsiness; symptoms also resemble atropine poi- 
soning, including dry mouth, fixed dilated pupils, 
fever, and flushed and reddened face. Children are 
particularly susceptible to the stimulating effects 
of antihistamines and can show excitement, hal- 
lucinations, toxic psychosis, delirium, tremors, 
and convulsions followed by respiratory or cardiac 
arrest. 

Treatment 

Induce vomiting followed by the administration of 
cathartics and activated charcoal. Perform gastric 
lavage for cases in which vomiting is not indicated, 
such as with poisoning with phenothiazine-type 
antihistamines, which are less responsive to ipecac- 
induced vomiting. 

antihypertensive drugs Medications prescribed to 
lower high blood pressure, they are also classified 
as belonging to one of several drug families accord- 
ing to the way they work. The subdivisions include 
drugs that increase the rate at which the body 
ehminates urine and salt (diuretics); beta adrener- 
gic blockers, drugs that block many of the effects 
of epinephrine (adrenahne) in the body; drugs that 
block the entry of calcium into the walls of the 
small arteries (calcium channel blockers); drugs 
that block formation of a natural body chemical 
and dilate small arteries (angiotensin-converting 
enzyme [ACE] inhibitors); and drugs that directly 
inhibit the effects of ACE II rather than block its 
production (ACE II inhibitors). ACE II inhibitors 
have actions similar to those of ACE inhibitors, but 
they appear to have a more favorable side effect 
and safety profile. 

Examples of antihypertensives according to drug 
class include: calcium-channel blockers nifedip- 
ine (Adalat) and verapamil (Calan); beta-blockers 
atenolol (Tenormin) and propranolol (Inderal); 
diuretic hydrochlorothiazide (Hydrodiuril); ACE 
inhibitors captopril (Capoten) and enalapril (Vaso- 
tec); and ACE II inhibitors losartan (Cozaar) and 
valsartan (Diovan). 

Symptoms 

In general, overdose causes a generalized depres- 
sion of the sympathetic nervous system, including 



lethargy, pinpoint pupils, slow heartbeat, low blood 
pressure, low fever, apnea, and coma. Onset of 
symptoms is usually within 30 to 60 minutes; full 
recovery occurs within 24 hours. 

Treatment 

Treatment for antihypertensive overdose includes 
induced vomiting or gastric lavage followed by 
the administration of activated charcoal and a 
cathartic. 

See also Aldomet; beta adrenergic block- 
ers; Catapres; diuretics; epinephrine; Minipress; 
quinidine. 



anti-inflammatory drugs These medications are 
used to reduce inflammation and include a wide 
variety of corticosteroids and nonsteroidal anti- 
inflammatory drugs (NSAIDS), such as aspirin 
and ibuprofen. Inflammation is one of the body's 
defense mechanisms in response to infection and 
certain chronic diseases such as rheumatoid arthri- 
tis. But as inflammation increases blood flow, it 
causes swelhng, redness, pain, and heat. Anti- 
inflammatory drugs are designed to combat this 
inflammation. 

Normally, anti-inflammatory drugs are not very 
toxic, but persons with gastrointestinal tract dis- 
ease, peptic ulcers, or poor heart function or those 
on anticoagulants should avoid them. 

Anti-inflammatory drugs include celecoxib 
(Celebrex), diflunisal (Dolobid), ibuprofen (Motrin, 
Rufen, Advil, Haltrain, Medipren, Nuprin, Tren- 
dar), fenoprofen (Nalfon), meclofenamate (Meclo- 
men) and naproxen (Anaprox, Naprosyn). None 
of these should be taken with other nonsteroid 
analgesics, or with warfarin or other oral antico- 
agulants, because bleeding time may be prolonged 
while on anti-inflammatory pain relievers. Antac- 
ids, however, may sometimes reduce the effects of 
an anti-inflammatory drug. 

Symptoms 

If a person is allergic to aspirin or other analgesic 
drugs, using another anti-inflammatory medicine 
could be fatal. Anti-inflammatory drugs become 
toxic when given to those with kidney prob- 
lems, since the kidneys cannot cleanse the blood. 



20 antimony 



Overdose causes kidney failure and severe liver 
reactions, including fatal jaundice. 

Normally, anti-inflammatory overdose produces 
mild stomach upset, with nausea and vomiting 
plus abdominal pain and internal bleeding. Occa- 
sionally, other symptoms might include sleepiness, 
lethargy, nystagmus (involuntary oscillation of the 
eyeball), tinnitus (ringing in the ears), and disori- 
entation. However, with some of the more toxic 
drugs and significant overdose of ibuprofen (in 
excess of 3,200 milhgrams per day), symptoms can 
include seizures, coma, metabolic acidosis, kidney 
and liver failure, and cardiorespiratory arrest. 

Treatment 

There is no antidote. Maintain symptomatic 
treatment together with antacids for mild stom- 
ach problems; perform gastric lavage, followed 
by administration of activated charcoal and a 
cathartic. 



antimony This silvery white soft metal is a popu- 
lar hardening agent used in the production of soft 
metal alloys and rubber, as a coloring agent and 
in flameproofing compounds. It is also contained 
in a wide variety of products, including batteries, 
foil, safety matches, ant paste, ceramics, textiles, 
glass, enamels, typesetting metals, and alloys. It is 
also used medicinally as an emetic and to combat 
worms. It is present in the dust and fumes pro- 
duced during mining and refining, and from the 
discharge of firearms. Stibine (antimony hydride) is 
a colorless gas produced as a by-product when ore 
containing antimony is treated with acid. 

A strong tissue irritant, antimony is lethal in 
doses of between 100 and 200 mg. Fatal poisonings 
from antimony are usually from drug overdoses, 
not from industrial exposure to vapors or dust. This 
is an extremely rare toxin. 

Poisonous part 

The toxic mechanism of both antimony and stibine 
is unknown, but its chemical action is similar to 
that of arsenic and arsine. It is believed that anti- 
mony compounds probably inactivate key enzymes 
in the body; stibine, like arsine gas, may destroy 
red blood cells. 



Symptoms 

While death is rare following the ingestion of 
antimony if the patient survives the initial gastro- 
enteritis, symptoms are unpleasant and include 
nausea, vomiting, and bloody diarrhea, with hepa- 
titis and kidney problems. Chronic antimony 
poisoning is quite similar to chronic arsenic toxic- 
ity, causing itchy skin, conjunctivitis, laryngitis, 
headache, anorexia, weight loss, and anemia. The 
inhalation of stibine causes headaches, weakness, 
nausea, vomiting, jaundice, anemia, and kidney 
failure. 

Treatment 

There is no specific antidote. As in arsenic poi- 
soning, treatment for ingestion involves gastric 
lavage followed by the administration of activated 
charcoal (although there is no evidence that this 
is effective). Do not use cathartics. Dimercaprol 
(to hasten the excretion of metals such as arsenic, 
gold, and mercury as well) may be administered, as 
well as narcotics for pain. Hospitahzation is recom- 
mended. In stibine poisoning, a blood transfusion 
may be necessary after massive destruction of red 
blood cells. 

See also arsenic; arsine gas. 

antipsychotic/psychometric drugs These drugs 
are used to treat psychosis, schizophrenia, bipo- 
lar disorder with psychotic manifestations, and 
agitated depression and are a common choice for 
suicide. They may also be used before surgery to 
ease fears, to treat tetanus, and to reheve behavior 
disorders in children. 

With the introduction of a new type of anti- 
psychotic drugs beginning in the 1990s, there are 
now two groups of antipsychotics. The conven- 
tional group include chlorpromazine (Thorazine), 
fluphenazine (Permitil), mesoridazine (Serentil), 
perphenazine (Trilafon), prochlorperazine, pro- 
methazine, thioridazine (Mellaril), trifluoperazine 
(Stelazine), thiothixene (Navane), haloperidol (Hal- 
dol), loxapine (Loxitane), and mohndone (Lidone). 
The second or atypical group consists of aripip- 
razole (Abilify), clozapine (Clozaril), olanzapine 
(Zyprexa), risperidone (Risperdal), and ziprosidone 
(Geodon). 



antivenin 21 



Symptoms 

These drugs seldom cause death because it takes 
a high dosage to reach toxic levels. There is also 
tolerance to the sedating effects, and patients on 
chronic therapy may tolerate much larger doses 
than normal. Therefore, the toxic dose after acute 
ingestion is quite variable. Severe intoxication 
may cause coma, seizures, and respiratory arrest. 
There may also be jaw muscle spasm, rigidity, 
and tremor. Further, patients on long-term anti- 
psychotic medication may develop a neuroleptic 
malignant syndrome (rigidity, high fever, sweating, 
lactic acidosis). 

Treatment 

There is no specific antidote. Some experts recom- 
mend bromocriptine in the treatment of neurolep- 
tic mahgnant syndrome, although other treatments 
for high fever are successful. Induce vomiting or 
perform gastric lavage if victim is seen within 30 to 
60 minutes or if the overdose is substantial (gastric 
lavage is preferred). 

The mainstay treatment for comatose patients 
is activated charcoal, intravenous fluids, and 
EGG monitoring; for patients with cardiotoxicity, 
it is plasma alkalinization with sodium bicar- 
bonate and hyperventilation; for neurotoxic- 
ity, it is intubation, plasma alkalinization, and 
hyperventilation. 

See also Thorazine. 



antiseptics and disinfectants Both products are 
designed to kill microorganisms; antiseptics are 
applied to living tissue and disinfectants to inani- 
mate objects. Despite the fact that they have never 
been proven to kill germs, they are widely used in 
both home and medical applications. Among the 
most common are hydrogen peroxide, alcohol, 
and iodine. All of these agents are generally used 
in diluted solutions and cause very little toxicity. 
Still, skin contact and vapors can be irritating to 
skin and the respiratory system. These products 
are more hazardous when used in aerosol form, 
since the mist can be inhaled through the nose 
and mouth. 

See also hydrogen peroxide; iodine; isopropyl 

ALCOHOL. 



antivenin A specific treatment for snake, scor- 
pion, spider, or other venomous animal bites. It is 
produced by inoculating animals (usually horses) 
with venom from a poisonous animal, which stim- 
ulates the production of antibodies in the horse to 
neutralize the poisons in the venom. A preparation 
with the antibodies (or antivenins) can then be 
produced from samples of the horse's blood. When 
given to a snakebite victim, the antibodies bind to 
and neutralize circulating venom proteins. 

Gommercial antivenins are available for bites 
from all types of pit vipers (rattlesnakes, cotton- 
mouth, and copperhead snakes) and the coral 
snake. Antivenins for treating the bites of scorpi- 
ons, spiders, fish, and jellyfish — or snakes that orig- 
inate outside the United States — can be obtained at 
zoos and from veterinarians. Black widow spider 
antivenin is available in some hospitals within the 
United States; antivenin for the stings of poisonous 
fish and jellyfish are generally not available in this 
country. 

Experts do warn that the two commercially 
marketed antivenins for snakebite available in 
this country cause painful and sometimes serious 
reactions in the vast majority of treated snakebite 
victims. While neither poses a life-threatening risk, 
both trigger a generalized and sometimes severe 
immunological reaction called "serum sickness" in 
about 75 percent of individuals. 

The most difficult aspect of producing antivenin 
lies in the purification — that is, extracting protein 
from the horse's blood that has the antibodies but 
not the other, useless proteins. These "useless" 
proteins from the horse are what trigger the seri- 
ous reactions when injected into humans, since 
the human immune system recognizes them as 
foreign. In response to these foreign substances, 
a few people go into anaphylactic shock, a life- 
threatening immune response characterized by 
flushing and itching, nausea, breathing problems, 
and lowered blood pressure. 

It is possible to test a snakebite victim's sensi- 
tivity to horse protein, but the skin test itself can 
trigger anaphylactic shock, and a positive response 
would then require a physician to choose between 
a potential severe reaction to antivenin and death 
or amputation from the snakebite. And in about 3 
percent of cases, victims with negative skin tests 



22 antivenin, black widow spider 



go on to have severe reactions to the antivenin 
anyway. 

Recent research suggests that high-tech purifi- 
cation techniques using sheep's blood or chiclten 
eggs instead of horse serum may resuh in a bet- 
ter antivenin. Chicken-based antibodies cannot 
trigger the highly inflammatory allergic reaction 
in humans that horse proteins can (unless there 
is a history of severe egg allergy); sheep antibod- 
ies also seem to cause fewer allergic reactions in 
humans. 

See also antivenin, black widow spider; anti- 
venin, CORAL snake; antivenin, rattlesnake; 

SNAKES, POISONOUS. 



antivenin, black widow spider The antidote for 
the bite of the black widow spider, this antivenin 
is produced by injecting horses with venom and 
collecting some of the blood, which then contains 
antibodies to the poison. The antivenin should 
be given to victims of black widow spider bite in 
the presence of uncontrolled severe high blood 
pressure or if the victim is pregnant. Black widow 
spider bites in pregnant women may cause an 
abdominal spasm so severe that it sets off a miscar- 
riage or early onset of labor. 

As with other types of antivenin produced from 
horse serum, immediate allergic reaction is pos- 
sible and a skin test for hypersensitivity should be 
performed. 

See also antivenin; black widow spider. 

antivenin, coral snake The antidote to the bite of 
the poisonous eastern coral snake (Micrurus fulvius) 
or the Texas coral snake (M. fulvius tenere). It is not 
effective against the bite of the Arizona or Sonora 
coral snake (M. euryxanthus). 

The antivenin is produced by injecting horses 
with venom and then collecting some of the 
blood, which contains antibodies to the poison. 
As with other types of antivenin produced from 
horse serum, immediate allergic reaction is pos- 
sible, and a skin test for hypersensitivity should be 
performed. 

See also antivenin; coral snake, Arizona; 
coral snake, eastern. 



antivenin, rattlesnake The antidote for rattlesnake 
bite is produced by injecting horses with the pooled 
venoms of the eastern diamondback rattlesnake, 
the western diamondback, the cascabel, or tropical, 
rattlesnake and the fer-de-lance. The blood serum 
from the horse then contains a combination of sev- 
eral antibodies against venom constituents. 

When given intravenously to the victim of 
rattlesnake bite, the antivenin binds to the venom 
throughout the body. However, it is possible to 
have an allergic reaction to the antivenin, causing 
anaphylactic shock even in those who tested nega- 
tive for horse serum allergy. 

See also antivenin; rattlesnakes. 

Antizol Antizol (fomepizole) is the first drug 
indicated as an antidote for antifreeze (ethylene 
glycol or methanol) poisoning. Commonly known 
as 4-MP (4-methylpyrazole), it works by blocking 
the formation of toxic ethylene glycol metabolites. 
If unchecked, these metabolites could lead to kid- 
ney damage. 

Side effects 

Reactions to the drug may include headache 
(14 percent), nausea (II percent) and dizziness, 
increased drowsiness and bad taste (6 percent) 
each. Minor allergic reactions have been reported. 

apomorphine This powerful emetic is an alka- 
loid salt derived from morphine. It has been used 
to induce vomiting in cases of oral poisoning, but 
at the moment, it is rarely used in either adult or 
childhood poisoning cases because it also strongly 
depresses breathing. Naloxone is used to treat the 
respiratory depression that occurs following apo- 
morphine use. Apomorphine is popular, however, 
in veterinary medicine. 
See also naloxone. 



apple of Sodom (Solanum sodomeum) This com- 
mon Hawaiian weed is also known as Dead Sea 
apple. It is a member of a very large genus of 1,700 
species, most of which have not been evaluated 
toxicologically. 



arrow poison frogs 23 



Poisonous part 

Human poisoning is usually attributed to imma- 
ture fruit, which contains the toxin solanine 
glycoalkaloid. 

Symptoms 

While there is little danger of fatal poisoning in 
adults, children may ingest a fatal amount of this 
plant. Symptoms appear several hours after inges- 
tion and include gastric irritation, scratchy throat, 
fever, and diarrhea. (Solanine poisoning is often 
confused with bacterial gastroenteritis.) 

Treatment 

The same general supportive care that would be 
given in gastroenteritis cases; fluid replacement 
may be required. 

apricot pit See Prunus. 

aquarium products According to numerous 
reports at poison control centers around the coun- 
try, a wide range of fairly nontoxic products sold 
for the upkeep of home aquariums may end up in 
the hands of young children, who may inadver- 
tently ingest them. In addition, adults may find 
them in medicine cabinets and use them mistak- 
enly for eye, ear, or nose drops. 

These products include antichlorine compounds 
(sodium thiosulfate), pH indicators, vitamins, cop- 
per sulfate, aquarium salts, and a range of antimi- 
crobials used to combat algae and fungi. Most are 
not very toxic, with the exception of some pH kits 
that contain sodium hydroxide (lye). 

See also alkaline corrosives. 



arrow poison frogs (Dendrobatidae and Phyllo- 

bates) This tree frog (also called "dart poison 
frogs") of the Colombian rain forest is one of a 
group of brightly colored amphibians of South and 
Central America. 

Once captured by the native people, it is car- 
ried back to camp, impaled on a sharpened stick 
and slowly roasted over an open fire; as it dies, 
the frog secretes a highly toxic mucus from the 



pores of its skin. This poison will later be applied 
to the tips of the Indians' blowgun darts and 
arrows. One specimen in this group is so toxic 
that one frog contains enough poison to kill about 
100 people; handling this frog with bare hands 
could be fatal. 

A supposed source of hunting magic in the rain 
forest, another type of this frog provides ointment 
used in prehunt ceremonies in which hunters burn 
themselves and then rub a stick coated with this 
frog's chemical on their wounds. According to leg- 
end, they awake with much keener senses the next 
morning. South American natives also rub frogs on 
wounds and cuts because the frog's skin contains 
potent antibiotic peptides. 

Secretions from still another type of toxic frog 
will change the color of parrots; rubbing a bit of 
frog secretion over the spot of a plucked feather 
will cause a new feather to grow back in a differ- 
ent color. 

Some poison frogs grow no bigger than a fin- 
gernail, whereas others vary so much in color that 
even frog experts mistake cousins as separate spe- 
cies. They all are rain forest inhabitants and live on 
land away from water, as long as there is enough 
water to lay their eggs. Most of these frogs have 
only slight water requirements, and some can be 
found living in the tiny water sac of bromeliad 
plants high above the forest floor. Most, however, 
prefer to live among the leaves that litter the rain 
forest floor, not in trees. 

All the arrow poison frogs are very small and 
beautifully colored and can be handled care- 
fully without danger — as long as they don't get 
excited. While there are many hundreds of differ- 
ent species, only a few are actually used to treat 
arrows; it takes up to 50 of them to coat the tips 
of a quiver. The most common of the poisonous 
arrow-tippers are 

Flat-spined Atelopus (Atelopus planispina), a gold and 
green Ecuadoran mountain frog with white 
spots and black markings. 

Zetek's frog (Atelopus zeteki), a Panamanian golden 
frog; males have black blotches. 

Yellow-spotted arrow poison frog (Dendrobates flavop- 
ictus), a black central Brazilian frog from the 
uplands, with bright yellow spots and lines. 



24 arsenic 



Boulenger's arrow poison frog (Atelopus boulengeri), a 

black mountain frog from Peru and Ecuador 

with creamy spots. 
Three-striped arrow poison frog (Dendrohates trivit- 

tatus), a South American black and yellow 

striped frog. 
Two-toned arrow poison frog (Phyilobates bicolor), 

a vivid red frog with black markings from 

northern South America. 
Gold arrow poison frog (Dendrohates auratus), a small 

gold and green frog from Nicaragua through 

Panama to Colombia. 

Poisonous part 

Of the family Dendrobatidae, four genera have 
skins with alkaloid compounds capable of killing 
a human if the toxin enters the blood (as from an 
arrow wound), and more than 50 poisonous spe- 
cies have been documented so far. Herpetologists 
suspect that the frog alkaloids are a by-product of 
metabolism. 

Symptoms 

While the toxin of the arrow poison frogs can be 
deadly if it enters the bloodstream (and one spe- 
cies, Phyilobates horribilus, can be fatal if chewed), 
skin contact with the frogs causes an irritating 
skin reaction, with swelling, reddening, and 
blistering. 

Treatment 

In cases of skin contact, wash secretions immedi- 
ately with soap and water. If a person touches the 
skin and rubs an eye, the eye should be immedi- 
ately rinsed with water or a saline solution. Signifi- 
cant skin reactions may require a doctor's care and 
treatment of dermatitis-type reaction; steroids may 
be helpful. 

arsenic [Other names: arsenic trihydride, arsenic 
trioxide, arsenous oxide, metallic arsenic, white or 
gray arsenic] The 20th most common element 
that occurs naturally in pure form, arsenic is pres- 
ent in all human tissue and is a fairly accessible 
poison. It is used in the manufacture of ceramics, 
enamels, paint, wallpaper, weed killer, insecticide, 
rat poisons, and pesticides. In its natural state. 



arsenic is a gray metal. While arsenic has been 
used intentionally to murder, poisoning also occurs 
as a result of industrial accidents or accidental 
ingestion. 

In addition, arsenic (present throughout the 
earth's crust) contaminates the groundwater 
around the world. In the United States, the Envi- 
ronmental Protection Agency (EPA) tightened the 
federal standards for arsenic by lowering the 50 
parts per billion (ppb) drinking water standard 
to 10 ppb. The new drinking water standard was 
adopted in January 2001, and the EPA gave public 
water utilities across the country five years (until 
January 2006) to reduce the level of arsenic in 
their tap water supplies. The standards apply to the 
approximately 74,000 community and noncom- 
munity water systems in the United States. 

Symptoms 

Most toxicologists believe arsenic combines with 
enzymes to interfere with cellular function, caus- 
ing severe gastric distress, esophageal pain, vomit- 
ing, and diarrhea with blood. The skin is cold and 
clammy, and blood pressure plummets followed by 
convulsions and coma. 

Arsenic poisoning can be chronic, occurring 
over a long period of time, and in such cases causes 
weakness, tiredness, scaly skin, and changes in skin 
pigmentation, followed by swelhng of the hning of 
the mouth and finally a degeneration of nerves, 
causing tinghng and numbness and moments of 
paralysis; death comes eventually from heart fail- 
ure, bone marrow failure, or infection. 

Poisoning may also result from a single large 
dose (acute poisoning), in which case death can 
come within a day, and sometimes after only a 
few hours. In acute cases, the arsenic affects the 
intestinal lining, quickly producing painful symp- 
toms — nausea, vomiting, diarrhea, sweating, and 
burning of the throat, followed by collapse and 
death. Individual susceptibility to arsenic poi- 
soning varies, and some individuals can develop 
a tolerance to doses of arsenic that would kill 
others. 

Because arsenic is an element and cannot be 
broken down any further, traces remaining in a 
person's hair, fingernails, and urine can be identi- 
fied upon urinalysis or autopsy. 



ascorbic acid 25 



Treatment 

In acute arsenic poisoning, the patient should be 
transported to a medical facility. Gastric lavage 
and fluid replacement are vital, together with the 
administration of dimercaprol for two or three days 
followed by penicillamine until the arsenic level in 
the urine drops. The victim should also be treated 
for dehydration, shock, pulmonary edema, and 
liver damage and may be put on a kidney dialysis 
machine after the dimercaprol. Chronic poisoning 
is also treated with dimercaprol. 

arsine gas This arsenic compound is an extremely 
poisonous, colorless inflammable gas (ASH3) com- 
posed of arsenic and hydrogen, which occurs when 
metals containing arsenic are exposed to acids. The 
gas, also called arsenic hydride, is used as a mili- 
tary poison gas, but most cases of arsine poisoning 
occur in the metallurgic industries during the refin- 
ing process and during galvanizing, soldering, and 
lead plating. 

According to the American Conference of Envi- 
ronmental Industrial Hygienists, 0.05 part per 
million is the maximum safe concentration for 
prolonged arsine exposure. 

Arsine gas has a disagreeable odor, similar to 
that of onions or carbide. 

Symptoms 

Inhalation causes vomiting, cramps, and nausea; 
decrease or cessation of urine output, which is 
often stained red four to six hours after exposure, 
followed by the appearance of jaundice. Effects of 
exposure to arsine gas include damaged kidneys 
and destruction of red blood cells; chronic expo- 
sure leads to gradual loss of strength, diarrhea or 
constipation, scaling of the skin that can become 
malignant, paralysis, confusion, and anemia. 

Treatment 

Physicians advocate early exchange transfusions 
and the administration of dimercaprol, which is 
usually not effective. Those with less than fatal 
doses of gas will recover; those who receive a fatal 
dose cannot be saved despite treatment. The only 
true solution to arsine gas poisoning is prevention. 
See also arsenic. 



artane See trihexyphenidyl. 



asbestos A mineral fiber found in rocks and man- 
ufactured into heat- and friction-resistant materi- 
als. Asbestos is one of the most widely recognized 
sources of environmentally produced disease. It 
was used in a wide variety of ceiling materials, 
insulation, roofing, shingles and siding, hair blow- 
ers, some vinyl floor tiles and vinyl sheet flooring, 
stoves and furnaces, appliance insulation, walls, 
and pipes. 

Unfortunately, the toxic nature of asbestos (it 
causes lung and stomach cancer) was not realized 
until the demand for its use resulted in its incorpo- 
ration in most buildings and vessels constructed for 
an entire generation. And even though it has been 
accepted that asbestos can cause disease in those 
exposed to it, there is considerable controversy 
about the dose required to produce disease. 

Occupations most at risk for asbestos exposure 
include insulators, shipyard workers, construction 
workers, and pipe fitters. 

Exposure to asbestos leads to an accumulation 
of the mineral in the lung, which then migrates to 
other regions in the body. It can cause asbestosis, 
a disease characterized by progressive restriction 
of lung capacity caused by a pulmonary fibrous 
reaction to the inhalation of asbestos fibers. Other 
diseases associated with asbestos exposure include 
lung cancer and mesothehoma (a rare tumor origi- 
nating in the cells lining the chest and abdominal 
cavity) . 

Asbestoslike fibers are commonly found in 
drinking water sources throughout the United 
States originating from rock areas in watersheds, 
from refuse dumps, and in asbestos-containing 
water pipes. There is no evidence, however, that 
ingesting these fibers causes disease in humans. 

If asbestos is found and must be disturbed, 
handle it carefully wearing a filtered mask. If at all 
possible, experts recommend that a trained con- 
tractor remove it. 



ascorbic acid (vitamin C) This is a powerful 
reducing agent used in treating methemoglobin- 
emia in conjunction with methylene blue following 



26 asp 



poisoning with benzene, lead or arsenic poison- 
ing, nicotine intoxication, bacterial toxins, and 
anaphylaxis. 

See also arsenic; benzene; lead poisoning; 

NICOTINE. 



asp See cobra, Egyptian. 

aspartame Sold under the trade names Nutra- 
Sweet Spoonful, Equal-Measure, and Equal, aspar- 
tame is an artificial sweetener discovered by accident 
in 1965. It is a synthetic combination of two amino 
acids (phenylalanine and aspartic acid). 

Although it was kept off the market for many 
years because one animal study suggested a high 
incidence of brain tumors, other studies failed to 
duplicate these results. Eventually it proved to 
taste better than many alternatives on the market, 
and it was subsequently approved for use as a food 
additive after being subjected to one of the most 
rigorous scientific safety testings. 

After more than 100 studies, however, there 
is still controversy over its safety. Critics say that 
many of the studies used by the Food and Drug 
Administration (FDA) to approve the use of aspar- 
tame are tainted by excessive food industry sup- 
port. But FDA reviews show no adverse health 
effects among laboratory animals tested. 

Yet complaints about aspartame accounted for 
between 78 and 85 percent of all complaints made to 
the Food and Drug Administration (FDA) from the 
1970s until 1992, when the FDA stopped categoriz- 
ing the complaints as a grievance against aspartame. 
Instead they put the complaints into general catego- 
ries such as "death" or "seizure" without mention- 
ing aspartame, even when the death or seizure was 
reported as a reaction to aspartame. The most com- 
mon complaint was that it caused severe headaches 
among sensitive users. In addition, aspartame can 
cause severe problems for people who have phe- 
nylketonuria (PKU) . Products using aspartame must 
carry a label to warn people with PKU disease that 
the product contains phenylalanine. 

According to the results of a review published 
in Critical Review of Toxicology in 2007, the studies 
evaluated provide no evidence to support an asso- 



ciation between aspartame and any type of cancer. 
The investigators concluded that the evidence 
from their review indicated that aspartame is safe 
at current consumption levels. However, another 
study, also pubhshed in 2007, reported the results 
of a carcinogenicity bioassay, which confirmed and 
reinforced the first experimental demonstration 
of aspartame's multipotential carcinogenicity at a 
dose close to the one deemed safe and acceptable 
for humans. The study also suggested that when 
exposure to aspartame begins at the fetal stage, 
the cancer-causing effects increase. Based on these 
findings, the National Institute of Environmen- 
tal Health Sciences recommended that the FDA 
reevaluate its position on aspartame as being safe 
under all conditions. 

Critics are also concerned about aspartame 
because it contains phenylalanine and aspartic 
acid, which in large doses excessively stimulate 
the brain, similar to the effect of monosodium glu- 
tamate (MSG). This overstimulation can damage 
the brain, perhaps leading to neurological diseases. 
Studies done on animals also suggest that children, 
especially infants, could be particularly vulnerable 
to brain damage caused by aspartate-induced over- 
stimulation of brain cells. For this reason, some 
scientists recommend that pregnant women avoid 
using aspartame since studies suggest that — at least 
in animals — infants are particularly vulnerable to 
brain damage caused by aspartate's excess stimula- 
tion to the brain. 

Because of a child's small body weight, aspar- 
tame doses per pound of body weight can easily 
be two to three times higher than that of an adult 
drinking, for example, the same amount of artifi- 
cially sweetened soft drink. 

While the long-term safety of aspartame has yet 
to be determined, large acute ingestions require 
only supportive therapy, if any. 

Aspergillus flavus A species of mold that pro- 
duces the very toxic substance aflatoxin. 
See also aflatoxins. 



aspirin (acetylsalicylic acid) This common pain- 
killer and antipyretic (fever reducer) is a slightly 



atropine 27 



bitter white powder usually sold in tablet form 
and, in correct dosages, is not poisonous. How- 
ever, in large doses (such as a child would take in 
swallowing a bottle of pills) it can cause acid-base 
imbalance, convulsions, coma and, occasionally, 
respiratory failure. 

Sahcyhc acid was first isolated from willow bark 
in 1838, but it was another 60 years before aspirin 
found its way into chnical practice. Since then, 
aspirin and other salicylates have been the most 
widely used medicines in the country. Because of 
this extensive use, it is not surprising that a large 
number of overdoses — both acute and chronic — 
have been recorded. 

In the United States, more than 200 differ- 
ent products contain acetylsalicylic acid (aspi- 
rin), sodium salicylate, and sahcylate acid itself. 
Salicylates are also found in a number of products 
designed for topical application, where they can 
lead to poisoning through absorption through the 
skin. 

There are a number of ways in which sahcy- 
late poisoning can occur. Because the metabolic 
pathways in young children are soon saturated by 
repeated excessive doses of sahcylates during ill- 
nesses accompanied by fever, it is fairly easy to give 
too much aspirin to young children. For this reason 
and because of the association between aspirin 
given during certain illness and Reye's syndrome, 
pediatricians usually prefer the use of acetamino- 
phen with young children. Frequent application of 
teething gels containing salicylates can also cause 
toxicity. In addition, deliberate suicide attempts 
by overdosing on aspirin are common in persons 
between ages 15 and 35 and sometimes occur in 
those as young as 8 or 10. 

However, according to the poison experts, the 
incidence of sahcylate poisoning is decreasing. 
Toxicity is decreasing, experts believe, primarily 
because less aspirin is being used by children and 
adults and because of child-resistant containers. 
Unfortunately, there has been a parallel trend of an 
increase in poisoning with acetaminophen, prob- 
ably because of increased use of this medicine. 

Symptoms 

Symptoms of overdose typically appear three to 
six hours after ingestion and usually involve the 



central nervous, lung, gastrointestinal, and renal 
systems. Aspirin in large doses can cause abdomi- 
nal pain, tinnitus (ringing in the ears), acid-base 
imbalance, fever, dehydration, and restlessness, 
while severe toxicity can result in lethargy, convul- 
sions, coma, and respiratory failure. 

Treatment 

Activated charcoal should be given as soon as pos- 
sible, and if bowel sounds are present, charcoal 
may be repeated every four hours until charcoal 
appears in the stool. Electrolyte abnormahties 
should be corrected, then alkahne diuresis (increas- 
ing production of urine) can be used to increase 
urine pH. In people who have ingested a large 
amount of salicylate, hemodialysis may be a very 
efficient way to eliminate it from circulation. 

atropine An alkaloid frequently found in differ- 
ent species of nightshade that can cause problems 
in swallowing or speaking, rapid heartbeat, dila- 
tion of pupils, and very high fever and delirium. 
Atropine is extracted from deadly nightshade (bel- 
ladonna) for medicinal purposes — as a premedi- 
cation before general anesthesia to lessen lung 
secretions, or as an emergency treatment for an 
abnormally slow heartbeat. Most homes, in fact, 
have medications containing atropine, since they 
are widely used for eye, skin, rectal, and gastroin- 
testinal problems. 

The fatal dose of atropine is unknown; while 
there is wide variance in tolerance from one person 
to another, estimates suggest that more than 20 
milhgrams is fatal to children and more than 100 
milhgrams fatal to adults. Jimsonweed-especially 
the seeds — is the plant most commonly ingested, 
usually to obtain a "high." 

In terms of benefits, atropine serves as an anti- 
dote for poisoning by organophosphate insecticides 
by treating SLUDGE (salivation, lacrimation, urina- 
tion, diaphoresis, gastrointestinal motility, emesis), 
the symptoms typical of organophosphate toxicity. 
Atropine is also an antidote for nerve gases, includ- 
ing Tabun, Sarin, Soman, and VX. Some nerve 
gases destroy acetylcholinesterase, which prolongs 
the action of acetylcholine. Atropine reduces the 
effect of acetylcholine. 



28 azalea 



Symptoms 

Symptoms of atropine poisoning include dry, burn- 
ing mouth; difficulty swallowing; thirst; blurred 
vision; hot, dry skin; fever and tachycardia. Fever 
can spike to 109°F in infants. Urinary problems, 
confusion, mania, dehrium, and psychotic behavior 
may continue for hours or days. With severe over- 
dose, death can occur following circulatory and 
respiratory collapse. 

Treatment 

The treatment for atropine poisoning involves the 
administration of physostigmine or pilocarpine. 



See also aldicarb; Aldomet; alkaloids; anti- 
histamines; benztropine; betel nut seed; Cata- 
PREs; Christmas rose; climbing lily; colocynth; 
death camas; digitoxin; fly agaric; henbane; 
Indian tobacco; jimsonweed; mandrake, Ameri- 
can; muscarine; nightshade, bittersweet; night- 
shade, DEADLY. 

azalea See rhododendron. 



Bacillus anthracis This bacterium forms spores 
that can cause a serious disease called anthrax. 
Bacillus anthracis is a zoonosis, which means it 
affects domestic and wild animals as well as 
humans. The fact that B. anthracis forms spores 
makes it especially difficult to control because the 
spores can exist for decades in a dormant state 
until they find an environment favorable for rapid 
growth. The ability of the spores to survive extreme 
conditions for prolonged periods of time is one of 
the main reasons this bacterium has been used by 
terrorists. 

Anthrax can appear in three different forms: 
cutaneous (skin), inhalational (lungs), and gas- 
trointestinal. Most cases (95 percent) are cutane- 
ous and they occur when the spores enter a cut 
or break on the skin when people handle prod- 
ucts from infected animals. About 20 percent of 
untreated cases of cutaneous anthrax result in 
death, and deaths are rare if appropriate antibiotic 
therapy is initiated. Inhalational anthrax is usually 
fatal, and even with aggressive treatment about 
50 percent of infected people die. It is contracted 
by breathing anthrax spores from infected animal 
products or, in the case of terrorism, by being delib- 
erately exposed to the spores, as occurred in the 
United States in 2001 when anthrax spores were 
mailed to various postal facilities. The gastrointes- 
tinal form of anthrax appears after consumption of 
contaminated meat. Deaths typically occur in 25 to 
60 percent of cases. 

Symptoms 

The range of symptoms differs depending on the 
type of anthrax that occurs. In skin anthrax, the 
first symptom is a small sore that develops into a 
blister, which then transforms into a painless ulcer 
with a black center. Other symptoms may include 



headache and malaise. A small percentage of cases 
becomes systemic and can be fatal. The warning 
symptoms of gastrointestinal anthrax are nausea, 
loss of appetite, bloody diarrhea, and fever, fol- 
lowed by stomach pain. Intestinal anthrax can 
become systemic and cause death. This form is 
rare in the United States. The most serious form 
is inhalational anthrax, which is marked by cold 
or flu symptoms followed by cough, chest dis- 
comfort, shortness of breath, muscle aches, and 
tiredness. Systemic infection has a mortality rate 
of nearly 100 percent. Symptoms for all three 
types of anthrax can appear within seven days 
of contact with the bacterium. For inhalational 
anthrax, symptoms can appear within a week or 
up to 42 days. 

Treatment 

To help prevent anthrax after exposure, antibiotic 
treatment (e.g., ciprofloxacin, levofloxacin, doxy- 
cycline, penicillin) combined with anthrax vac- 
cine is critical and should be started immediately. 
Treatment after infection has occurred involves a 
60-day course of antibiotics. After acute symptoms 
have appeared, antibiotics can kill the bacteria but 
will not affect the toxins that have formed. The 
effectiveness of treatment depends on the type of 
anthrax and how quickly treatment was initiated. 
Individuals may die within two to three days from 
respiratory failure, sepsis, and shock. 

Prevention 

An anthrax vaccine has been developed and is 
reportedly about 93 percent effective in preventing 
the disease. Immunization is not recommended for 
everyone. The Advisory Committee on Immuni- 
zation Practices recommends the vaccine for the 
following people: those who work directly with 



29 



30 Bacillus cereus 



the organisms in laboratories; those who work 
with imported animal furs or hides in areas where 
standards are not sufficient to prevent exposure to 
anthrax; people who handle potentially infected 
animal products in countries where incidence is 
high; and military personnel who are in areas with 
high risk for exposure to the organism. Pregnant 
women should be vaccinated only if absolutely 
necessary. 

The immunization consists of three injections 
given two weeks apart, followed by three addi- 
tional injections administered at six, 12, and 18 
months. Annual booster injections are recom- 
mended thereafter. 



Bacillus cereus The Bacillus cereus bacteria multi- 
plies in raw foods at room temperature, producing 
heat-resistant toxins most often found in steamed 
or refried rice. While occurrence is less common 
in the United States, it's likely that episodes are 
underreported because symptoms are so similar to 
other types of food poisoning. It's most commonly 
found in cereals (especially rice), vegetables, and 
pasta. 

Symptoms 

These bacteria produce two distinct types of food 
poisoning: The first features a short incubation 
period after eating tainted food (usually less than 
six hours), causing cramps and vomiting and 
occasionally a short bout of diarrhea. Almost 80 
percent of patients with these symptoms who test 
positive for B. cereus poisoning have eaten steamed 
or refried rice at Chinese restaurants. The second 
type appears within eight to 24 hours after inges- 
tion of tainted food and causes abdominal cramps 
and diarrhea with very little vomiting. 

The illness is usually mild and self-limiting. 

Treatment 

There is no specific therapy beyond treating 
symptoms. 

Prevention 

Keep preparation surfaces clean, and don't allow 
leftovers to remain in the open air for long. Heat 
leftovers quickly, and eat them right away. 



Bacillus thuringiensis (Bt) A popular botanic insec- 
ticide, Bt is a species of bacterium sold in a variety of 
strains and it kills soft-bodied insects or those in their 
larval form. The most widely used strain kills larval 
caterpillars of many moths, including the gypsy 
moth, the cabbage moth, and the berry moth. Newly 
developed strains are aimed at beetle larvae (such 
as bean beetles and potato beetles), while others are 
aimed at borers. Some Bts from specialty stores com- 
bine the different strains into one superpesticide. 

Bt will also kill some beneficial insects, but only 
in the soft-bodied larval stage. The Environmental 
Protection Agency (EPA) has declared Bt to be safe 
for humans and other mammals, birds, and fish. It 
is safe enough to be exempt from food residue tol- 
erances, endangered species labeling, and ground- 
water restrictions. 

See also botanic insecticides; pesticides. 



BAL (2,3-dimercaptopropanol, dimercaprol, British 
anti-lewisite) An antidote for mercury, copper, 
arsenic, gold, nickel, lead, and antimony poisoning, 
but less effective for silver poisoning. It may make 
iron, selenium, or cadmium poisoning worse, since 
BAL complexes act on the liver. It is best given as 
soon as possible following ingestion of the toxic 
substance. 



baneberry (Actaea) [Other names: black bane- 
berry, cohosh, doll's eyes, European baneberry, 
herb-Christopher, necklaceweed, snakeberry, west- 
ern baneberry] This plant of the buttercup family 
includes eight species of perennial herbs that grow 
less than 2 feet tall in richly wooded areas, boasting 
oversize leaves each with two or more leaflets. In 
warm weather (usually spring) this herb is adorned 
with distinct bunches of pearly white flowers at the 
tips of the stems. The fruit matures in late summer 
or early fall. 

The white baneberry (A. pachypoda or A. alba) 
has snow-white fruit and is native to North Amer- 
ica. The red baneberry or red cohosh (A. rubra) is 
another North American native and bears a red or 
ivory fruit. Cohosh, or herb Christopher (A. spicata), 
resembles A. rubra and has dark purple fruit some- 
times used to make dye. 



barbiturates 31 



A. pachypoda thrives from Nova Scotia, Canada 
south along the east coast of the United States as 
far as Georgia, west to Missouri and north to Min- 
nesota. A. rubra grows throughout Canada and the 
United States. A. spicata is cultivated in Canada and 
the United States. 

Poisonous part 

Only the red or white berries, foliage, and roots 
contain the unknown toxin, which is a fast-acting 
and deadly poison acting on the heart. The root is a 
violent purgative, irritant, and emetic. In mountain 
forests, the black berries are often confused with 
blueberries. While no loss of life has been reported 
in the United States, European children have died 
after eating baneberry fruit. 

Symptoms 

Prolonged contact with the skin causes skin rash. If 
the plant is eaten, symptoms begin within several 
hours to a few days, with excruciating pain and 
inflammation followed by bhsters or open sores 
of the lips, tongue, mouth, and throat. Larger 
amounts of the plant cause vomiting streaked with 
bright-red blood; severe diarrhea and relentless 
abdominal cramps; excessive, blood-tinged urine; 
dizziness; fainting; and mental confusion or hal- 
lucinations. In critical cases, there are grand mal 
seizures. 

Prognosis is guarded; often, the electrolytes 
and fluids of the body are depleted, and the kid- 
neys and nervous system can sustain permanent 
damage if the symptoms are severe or prolonged. 
Death may follow if the poison is not cared for 
immediately. 

Treatment 

The irritating effects of this plant usually limit the 
amount ingested. Gastric lavage should be per- 
formed followed by the administration of milk or 
egg white as a demulcent. Renal function and fluid 
and electrolyte levels should be monitored. 

Barbados nut (Jatropha curcas) [Other names: 
curcus bean, kukui haole, physic nut, purge 
nut] This small, spreading shade tree grows to 
about 15 feet and is found in southern Florida 



and Hawaii, Africa, Mexico, Asia, and Central 
and South America. Its flowers are small and 
green yellow, with three to five lobed leaves; it 
also produces a sticky sap. A resinous substance 
produced by insects feeding on the leaves is used 
to make a varnish for guitars. Jatropha is a genus 
of the spurge family found in both the Old World 
and New World, containing about 125 species of 
herbs, shrubs, and trees. 

Unfortunately, while the seeds contained in the 
nut of this tree are extremely tasty, they contain 
more than 55 percent of an oil more potent than 
castor oil. In tropical areas the seeds are still used by 
folk healers, although they are quite dangerous. 

Poisonous part 

All parts of the Barbados nut contain the poison 
jatrophin, which is a harsh purgative. The poison 
kills by interfering with the synthesis of protein in 
intestinal wall cells. The seeds can be eaten if thor- 
oughly roasted to remove the poison. 

Symptoms 

This plant is quickly fatal; within 1 5 to 20 minutes, 
symptoms appear: burning throat, bloating, dizzi- 
ness, vomiting, diarrhea, drowsiness, leg cramps, 
difficulty breathing. May be fatal to children. 

Treatment 

Gastric lavage (unless there has been a great deal of 
vomiting already). Rehydration. 
See also coral plant. 



barbiturates A group of sedative drugs including 
pentobarbital (Nembutal), phenobarbital (Luminal 
or "downers"), secobarbital (Seconal or "reds"), 
thiopental (Pentothol), and amobarbital (Amytal), 
that work by depressing brain activity. Overdosing 
on barbiturates is a common cause of death from 
suicide. Because these drugs are highly addictive 
and often abused, their use today is strictly con- 
trolled. Overdose — particularly when used with 
alcohol — is common. The toxicity of a particular 
type of barbiturate depends on how quickly it is 
designed to act. All cause unconsciousness, and 
their effects depend in part on how well the liver 
metabolizes them. 



32 barium 



Symptoms 

Within 30 minutes (usually much sooner) sedation 
begins, followed by dizziness, headache, confusion, 
heart irregularities, low blood pressure, and then 
coma, which may last up to several days. While the 
toxicity level for barbiturates is high, they can be 
fatal in combination with alcohol. 

Treatment 

There are no direct antidotes to barbiturates. Bar- 
biturates are quickly absorbed in the system, so 
gastric lavage needs to be performed no later than 
the first few hours after ingestion if treatment is 
to be effective. Even when it is performed quickly, 
however, often little of the drug is retrieved this 
way. This may be followed by repeated doses of 
activated charcoal. Fatality from barbiturate over- 
dose ranges between 5 and 7 percent, but many 
people attempt suicide again using barbiturates. 
For this reason, follow-up mental health care is 
strongly recommended. 

barium While barium poisonings are not com- 
mon, they are usually due to accidental contami- 
nation of food or a result of suicide. Water-soluble 
barium salts (barium acetate, carbonate, chlo- 
ride, hydroxide, nitrate, sulfide) are extremely 
toxic, but the insoluble salt barium sulfate is not 
because it cannot be absorbed. The soluble bar- 
ium salts are used in fireworks, depilatories, and 
rat poisons, and are used to manufacture glass 
and to dye textiles. 

Symptoms 

Within minutes to a few hours after ingestion, 
victims experience muscle weakness, followed by 
paralysis of the hmbs and lungs, with additional 
heart problems. There may also be gastroenteritis 
with watery diarrhea, impaired vision, and central 
nervous system depression. However, victims usu- 
ally remain conscious. 

Treatment 

Symptomatic treatment, with the administration 
of potassium chloride. Induce vomiting or perform 
gastric lavage; administer activated charcoal and a 
cathartic. 



bee stings For most Americans, a bee sting is a 
minor annoyance and can be fatal only if occur- 
ring in large numbers (hundreds in an adult). But 
between 1 million and 2 million Americans are 
severely allergic to the inflammatory substances 
in the venom of bees, wasps, hornets, and yellow 
jackets — which means they have been sensitized 
by the venom from a sting in the past so that a 
single subsequent sting could provoke a severe 
allergic reaction. 

Bee stings cause three to four times more deaths 
in the United States than do snake bites, but the 
deaths are related to an individual's sensitivity, 
not the relative toxicity of any one insect poison. 
About 50 to 100 Americans die each year from bee 
stings. Since the bee venom toxicity is related to an 
individual's sensitivity and not to the venom itself, 
there is no bee antivenin available. 

In the case of Africanized honey bees, it is 
often the large number of bee stings, as well as an 
individual's sensitivity, that causes death. Their 
venom is no more potent than that of native 
honey bees, but Africanized bees generally attack 
in great numbers and will pursue their prey long 
distances. They also will attack with little provo- 
cation, reacting to vibrations from a vehicle or 
noises, although many attacks occur when people 
disturb a hive. The first Africanized bee swarm in 
the United States was seen in October 1990. In 
July 1993, an 82-year-old man in Texas became 
the first person to die in the United States from 
Africanized honey bee stings after being stung 
more than 40 times. 

While hornets and wasps usually do not attack 
unless their nest is threatened, yellow jackets are 
very aggressive and quick tempered. Of all the 
stinging insects, the most lethal is the wasp. The 
vicious hornet or yellow jacket (striped yellow 
and black) is so aggressive that it both stings and 
bites. Honeybees have round, smooth abdomens; 
bumblebees are two to three times larger than 
honeybees and have round, furry abdomens. Hor- 
nets, yellow jackets, and wasps have long, slender 
abdomens and are all usually striped yellow and 
black. 

A bee sting activates the body's immune sys- 
tem, which releases antibodies that counteract 
the harmful effects of germs and toxins. However, 



bellyache bush 33 



some individuals release too much of this antibody, 
which can become life threatening. 

Allergic reactions to bee stings, therefore, are 
more common in adults than in children because 
adults have had more of a chance to develop a 
serious allergy to the stings. Each subsequent sting 
usually results in a more serious allergic reaction in 
those already sensitized. 

The severity of a sting also depends on where 
it is located on the body: A sting to the neck can 
affect breathing, and swallowing a bee can cause 
strangulation if the bee stings the inside of the 
throat. 

Certain types of clothing can be good protection 
against a bee sting; white or light-colored clothing 
with a smooth finish is less likely to excite bees 
to attack. Leather is particularly irritating to bees, 
but they will also become disturbed with brightly 
colored, dark, rough, or wooly material. Bees also 
seem to become irritated over perspiration odors, 
perfumes, suntan lotions, and hair sprays. 

To avoid being stung by bees, wasps, yellow 
jackets, and hornets, it is best to remain motionless 
and not to wave or swing your arms but to retreat 
slowly while protecting your face with your hands, 
or if possible to lie face down on the ground. An 
exception is an attack by Africanized honey bees 
or any colony of bees, in which case you should 
run and protect your head and face, which are the 
main targets of Africanized bees. If necessary, pull 
your shirt up over your head and seek shelter as 
quickly as possible. 

Symptoms 

When stung, allergic individuals experience sore- 
ness and swelling not only at the site of the sting 
but on other parts of the body as well. Symptoms 
in those allergic to bee stings include fever, chills, 
light-headedness, hives, joint and muscle pain, 
swelling of the lymph glands, and bronchial con- 
striction. Other severe reactions include a sudden 
drop in blood pressure with loss of conscious- 
ness, difficulty breathing, shock and, occasionally, 
death within one hour. Multiple stings — 30 or 40 
insects — will cause a reaction even in an unsensi- 
tized individual, including chills, fever, vomiting, 
pulmonary edema, difficulty breathing, drop in 
blood pressure, and collapse. 



Treatment 

A bee will often leave its sting sac in the wound; 
thus to treat a sting, remove the stinger by scrap- 
ing it away with a fingernail or the edge of a 
knife blade. Grasping it with tweezers will sim- 
ply squeeze more venom into the wound. Wash 
the wound with soap and water and apply anti- 
septic and a cold compress; ice will help reduce 
swelling. 

Pain and irritation can be relieved by applying 
a paste made from either baking soda and water, 
or meat tenderizer and water. The meat tender- 
izer, developed to break down meat protein, also 
neutralizes bee venom. For stings in the mouth or 
throat, give victim ice cubes to suck while seeking 
medical attention. 

Those who have had a severe reaction should 
carry an emergency self-treatment kit, available 
only with a doctor's prescription, containing anti- 
histamine tablets, alcohol swabs, and a preloaded 
syringe with epinephrine, which counteracts the 
allergic response of the sting. Diphenhydramine 
(Benadryl) can stop or slow symptoms, but it must 
be given immediately. 

In addition, highly sensitized individuals may 
consider taking immunotherapy, but since this 
procedure carries a risk of anaphylactic shock, it 
should only be administered by a physician with 
access to epinephrine. 



bellyache bush (Jatropha gossypiifolia) This 
annual found throughout the New World is a 
member of a large genus of shrubs or small trees 
with a three-sided seed capsule. 

Poisonous part 

The seeds are poisonous and contain a variety of 
toxins and cathartic oils. Ingestion of just one seed 
can be serious. The toxins inhibit protein synthesis 
in cells of the intestinal wall and may cause serious 
or fatal poisoning. 

Symptoms 

The onset of symptoms (nausea, vomiting, and 
diarrhea) occurs rapidly, unlike poisoning with 
other plants with toxic lectins. 



34 benzene 



Treatment 

Treat symptoms; give fluids. 

benzene This simple aromatic hydrocarbon is a 
common household solvent used as a cleaning agent 
for rubber, fats, grease paints, and lacquers and is 
a known carcinogen. Because of this, it has widely 
been replaced by toluene in many industrial prod- 
ucts. It is no longer available for home or private 
use. Benzene is obtained from coke-oven gas or from 
petroleum, and it is highly toxic. Long-term expo- 
sure may lead to acute leukemia and aplastic ane- 
mia. Most cases of benzene poisoning are caused by 
skin contact or breathing fumes in poorly ventilated 
rooms; recent cases have been reported of fatalities 
following cleaning of tank cars. It may even occur 
after sniffing gasoline with a high benzene content. 

Symptoms 

Symptoms are caused by stomach irritation and 
benzene's depressive action on the body's central 
nervous system and bone marrow. Breathing these 
solvent fumes can cause headache, eye irrita- 
tion, dizziness, visual disturbances, nausea, and 
euphoria; more toxic cases include tremors, delir- 
ium, unconsciousness, coma, and convulsions. In 
extreme cases, inhaling these fumes can be fatal. 

Chronic cases of breathing benzene fumes cause 
a diminished production of all blood components 
and can lead to weakness, anorexia, and anemia, 
with abnormal bleeding. In cases of chronic poi- 
soning, symptoms may not appear until months 
or years after contact — even after exposure to ben- 
zene has ceased. 

Treatment 

Call the poison control center before attempting 
any treatment. If fumes have been inhaled, get the 
victim into fresh air and give artificial respiration if 
needed. For skin contamination, rinse in running 
water for at least 1 5 minutes. 



benzene hexachloride [Other names: gamma- 
hexane; 1,2,3,4,5,6-hexachlorocyclohexane; BHC; 
DBH; HCCH; HCH; trade name Streunex] This 
synthetic pesticide is found in a white crystalline. 



wettable powder, emulsion, dust, and solution in 
organic solvents. Both benzene hexachloride and 
lindane are moderately toxic when inhaled or 
absorbed and extremely poisonous if ingested. Dis- 
agreeable in odor, benzene hexachloride does not 
dissolve in water but is readily soluble in fats or oils 
and is therefore particularly dangerous if ingested 
after a fatty meal. Benzene hexachloride is widely 
used by veterinarians to combat fleas and ticks. 

Symptoms 

Benzene hexachloride affects the central nervous 
system and may cause liver and kidney damage. 
Symptoms appear within 30 minutes to three 
hours, although it may take as long as six hours 
before reactions appear. When benzene hexachlo- 
ride is ingested, mucous membranes that touched 
the poison become irritated, followed by vomit- 
ing, diarrhea, and convulsions. Poisoning may 
be fatal, usually as a result of pulmonary edema. 
Bread tainted with HCH has sickened some people, 
including infants breastfed by women who have 
eaten the bread. Because benzene hexachloride is 
rapidly excreted by the body, chronic poisoning is 
unlikely. 

Treatment 

Symptomatic treatment. 

benzodiazepines A class of drugs containing 
compounds that vary widely in their strength, 
duration, and chnical use. In general, they are 
given as muscle relaxants, to relieve short-term 
anxiety due to stress or trauma, to relieve the 
unpleasant delirium of alcohol withdrawal, and 
to help induce sleep. Fatalities from overdose of 
a benzodiazepine are rare, unless the drug is used 
with other central nervous system depressants 
(such as alcohol or barbiturates). 

Benzodiazepines include Ativan (lorazepam), 
Centrax (prazepam), Dalmane (flurazepam), Lib- 
rium (chlordiazepoxide), Serax (oxazepam), Tranx- 
ene (chlorazepate), and Valium (diazepam). 
Newer potent short-acting agents include Halcion 
(triazolam), Xanax (alprazolam), and Versed (mid- 
azolam). Rohypnol (flunitrazepam) is a benzodi- 
azepine that is not legal in the United States but 



beryllium 35 



which is a drug of abuse, specifically as a date rape 
drug. 

Symptoms 

Most benzodiazepines are addictive, and all can be 
either taken by mouth or injected; a few are avail- 
able as suppositories. In general, overdose symp- 
toms include drowsiness, weakness, crossed eyes, 
double vision, uncoordination, and lassitude, fol- 
lowed by convulsions, coma, cyanosis, and breath- 
ing problems. Chronic abuse can produce a skin 
rash, stomach problems, headaches, and blurred 
vision. In all of these drugs, symptoms can appear 
within a few minutes to several hours. Respiratory 
arrest is more common with the shorter-acting 
drugs (Xanax, Versed, and Halcion). 

Treatment 

The administration of flumazenil (Mazacon) can 
quickly reverse a coma caused by benzodiazepine 
overdose. 

See also Dalmane; diazepam; midazolam. 

benztropine (Cogentin) This is an antidote to 
many of the extrapyramidal side effects (wobbly 
gait, slurred speech, foaming at the mouth, forget- 
fulness, drooling, stiffness) sometimes seen with 
large doses of psychiatric drugs. It is pharmacologi- 
cally similar to atropine. 
See also atropine. 



benzylpiperazine [Street names include BZP, A2, 
Legal E, Legal X] First synthesized in 1944, ben- 
zylpiperazine was a potential antiparasitic drug 
that was later found to have both antidepressant 
and amphetamine-like properties, but it was never 
developed for the general market. Benzylpipera- 
zine has become favored by drug abusers because 
of its amphetaminehke effects, and since 1996 it 
has been classified as a Schedule I controlled sub- 
stance by the Drug Enforcement Administration. 

Benzylpiperazine is usually taken orally as a 
powder, tablets, or capsules; it can also be smoked 
or snorted. Some abusers take it along with I- 
(3-trifluoro-methyl phenyl)piperazine (TFMPP), a 
noncontrolled substance, in an effort to enhance 



its effects. Benzylpiperazine is sometimes used as 
a substitute for MDMA (methylenedioxymetham- 
phetamine, or ecstasy) at raves because it reportedly 
causes arousal, euphoria, and a general feeling of 
well-being. 

Symptoms 

Benzylpiperazine produces a severe hangover effect 
after the drug wears off. Other side effects include 
dry mouth, urine retention, and dilated pupils. 
Effects of long-term use include confusion, irregu- 
lar heartbeat, memory problems, and impotence, 
while typical overdose effects include psychotic 
episodes and seizures. 

Treatment 

Symptomatic. In New Zealand, where benzylpipera- 
zine is legal, some manufacturers offer recovery pills, 
which contain vitamins and 5-HTP, which allegedly 
ease the hangover effect benzylpiperazine produces. 
See also ecstasy. 



beryllium This hard, grayish metal is found natu- 
rally in coal, soil, mineral rocks, and volcanic dust. 
Beryllium compounds are mined and the beryllium 
is used in nuclear weapons and reactors, instru- 
ments. X-ray machines, mirrors, and aircraft and 
space vehicles. Beryllium ores are used to make 
ceramics for high-technology applications, while 
beryllium alloys are used in computers, sports 
equipment, automobiles, and dental bridges. 

People who work in or live near beryllium 
industries have the greatest potential for exposure 
to the metal. Beryllium can harm the lungs if it is 
breathed in; the extent of the damage depends on 
the degree and length of exposure. Up to 15 per- 
cent of people who are exposed to beryllium on the 
job become sensitive to it and may develop chronic 
beryllium disease, an irreversible and sometimes 
fatal disease in which the lungs are scarred. Long- 
term exposure to beryllium can increase the risk of 
developing lung cancer. 

The International Agency for Research on Can- 
cer and the Department of Health and Human Ser- 
vices have determined that beryllium is a human 
carcinogen. The Environmental Protection Agency 
has categorized berylhum as a probable human 



36 beta adrenergic blockers 



carcinogen and estimated that lifetime exposure to 
0.04 ug/m' beryllium can result in a one in 1,000 
chance of developing cancer. 

Berylhum enters the environment as dust from 
burning oil and coal and from industrial waste. The 
dust eventually settles on the earth and water, and 
the beryllium in industrial waste often ends up in 
waterways, where some of the compounds dissolve 
in water while most of them settle to the bottom. 

Symptoms 

People who develop chronic beryllium disease may 
be asymptomatic or begin with coughing, chest 
pain, shortness of breath, weakness, anorexia, 
and/or fatigue. The disease can also lead to right 
side heart enlargement and heart disease. Swal- 
lowing beryllium does not appear to cause effects 
in humans because only a minute amount of the 
metal is absorbed. 

Treatment 

Currently there is no cure for chronic beryllium 
disease, but treatment can help slow progression of 
the disease and prevent additional damage to the 
lungs. Immunosuppressive drugs such as predni- 
sone are often prescribed because they help relieve 
symptoms while improving gas exchange between 
the lungs and the blood. Because prednisone 
can cause significant side effects, use of this drug 
should be discussed with a healthcare provider. 
Another option is oxygen therapy, which can be 
delivered via oxygen concentrators, compressed 
gas systems, or liquid systems, depending on the 
patient's needs. In serious circumstances, lung 
transplantation may be the only solution. 

beta adrenergic blockers These "beta blockers " 
slow the heart rate and reduce the force of the 
heart muscle's contraction and are used to treat 
high blood pressure, arrhythmias, angina, migraine 
headaches, and glaucoma. There are a wide variety 
of beta blockers, including Tenormin, Lopressor, 
Visken, and Inderal. People with asthma should 
not take beta blockers. 

Symptoms 

Unfortunately, the response to beta blockers var- 
ies from patient to patient, depending on overall 



health and other medications; it is possible to have 
a fatal reaction to even a normal dose. Ingestion of 
only two or three times the therapeutic dose should 
be considered to be potentially fatal for any patient. 
In addition, the sudden withdrawal of beta blockers 
can cause heart failure, especially in patients who 
have problems with the aorta. Many patients who 
overdose on beta blockers may also be taking other 
cardioactive drugs or have an underlying heart 
problem, both of which may worsen the effects 
of the overdose. Overdoses with beta blockers all 
have similar symptoms and toxicity ratings. 

Treatment 

Symptomatic treatment; perform gastric lavage 
(vomiting is not recommended because of the 
danger of seizures and coma). Administer activated 
charcoal and a cathartic. A glucagon bolus can be 
diagnostic and therapeutic as well. In severe cases 
of atenolol overdoses, hemodialysis may be useful; 
nadolol and sotalol are also reportedly removed by 
hemodialysis, while propranolol, metoprolol, and 
timolol are not. Hemodialysis should be considered 
only when treatment with glucagon and other 
pharmacotherapy are not successful. 

betel nut seed (Areca catechu) This poisonous 
seed is chewed for its narcotic effects by native peo- 
ples in central and southwestern Asia and South 
America, but too large an amount can be toxic. 

Poisonous part 

The seeds are considered extremely poisonous 
and contain the toxic alkaloid arecain and other 
poisons. 

Symptoms 

Within 20 minutes of ingestion, patients expe- 
rience vomiting, diarrhea, difficulty breathing, 
impaired vision, convulsions, and death. 

Treatment 

Antidote is atropine. 

birth control, botanical From earhest times, 
people have searched for an herbal remedy for 



black locust 37 



unwanted pregnancy; unfortunately, most plants 
capable of killing a fetus are also capable of killing 
the mother. The Amazon Indians chew the leaves 
of several jungle plants for contraceptive purposes, 
and the Chinese have used abortifacients since the 
ninth century. 

According to Aristotle, oil from the cedar and 
olive prevent conception; in medieval times, onion 
juice smeared on the penis was supposed to work. 
Abortifacients over the centuries include thyme, 
rue, mugwort, ergot, iris, and pennyroyal; a chemi- 
cal from the English yew was so widely used for 
abortion that the plant was known as the "bastard 
killer." 

See also ergot; pennyroyal oil; yew. 

birth control pills Medication containing pro- 
gesterone or estrogen (or derivatives) used for the 
prevention of pregnancy. At present, they are not 
considered toxic when ingested accidentally by 
children. 



bisphenol-A Also known as BPA, bisphenol-A 
is a controversial plastic chemical that may or 
may not pose a health hazard, depending on 
which research and/or researchers people choose 
to believe. Bisphenol-A, which is found in polycar- 
bonate plastic and in epoxy resins, is used in a wide 
range of products, from water and baby bottles 
to the lining of metal products (including cans 
for food), a plastic coating for children's teeth to 
prevent cavities, refrigerator shelving, microwave 
ovenware, and eating utensils. It is also found in 
flooring, enamels and varnishes, adhesives, artifi- 
cial teeth, nail pohsh, compact discs, and in parts of 
automobiles, tools, electrical appliances, and office 
instruments. High levels of bisphenol-A are known 
to disrupt hormone levels in the body. 

There are two main views on the safety of 
bisphenol-A. One is that the plastic poses virtually 
no health threat. That is the opinion the European 
Food Safety Authority (EFSA) and the Food and 
Drug Administration took in summer 2008. The 
EFSA reviewed the research on bisphenol-A, much 
of which has been done on rodents, and concluded 
that bisphenol-A passes through the human body 



much faster than it does in rodents and thus there 
is little chance that it can harm humans. This view 
conflicts with that of the U.S. government scien- 
tists at the National Toxicology Program (NTP), 
who said that based on results of studies done in 
rodents, there was concern about bisphenol-A 
because animal studies suggested low doses can 
cause changes in behavior and the brain, and that 
it may reduce birth weight and survival in fetuses. 
The NTP report initiated publicity which prompted 
questions among the general public about the 
safety of bisphenol-A and for some major retailers, 
including Wal-Mart, who decided to turn away 
baby bottles that contain bisphenol-A. 

Other experts state that bisphenol-A poses at 
least a reasonable threat to health and thus should 
be banned, or, at the least, exposure should be 
severely limited. Canadian health officials, for 
example, announced their intention to ban the use 
of the chemical in baby bottles, and state and fed- 
eral lawmakers have introduced legislation to ban 
the chemical's use in products made for children. 
As of August 2008, California and at least ten other 
states were considering bills to restrict use of the 
chemical. More than 6 billion pounds of the chemi- 
cal are produced in the United States each year. 

According to laboratory tests spearheaded by the 
Environmental Working Group in 2007, more than 
50 percent of 97 cans of commonly eaten foods 
that were evaluated contained bisphenol-A. Ten 
percent of all canned food tested and 33 percent 
of infant formula tested contained enough BPA to 
expose a woman or infant to BPA levels more than 
200 times the government's traditional safe level of 
exposure for industrial chemicals. Unfortunately, 
the government has not set safety standard hmits 
for BPA in canned food, even though scientists 
have found exceedingly high levels in so many of 
these items. According to the Centers for Disease 
Control and Prevention, about 93 percent of Amer- 
icans have traces of bisphenol in their urine. 

black locust (Robinia pseudoacacia) [Other 
names: bastard acacia, black acacia, false acacia, 
green locust, pea flower locust, post locust, silver 
chain, treesail, white honey flower, white locust, 
yellow locust.] The towering locust tree can grow 



38 black snake, Australian 



to be 80 feet tall and is found particularly in the 
eastern United States from Pennsylvania through 
Georgia, in the Smoky Mountains and the Ozarks. 

Its compound leaves have a series of leaflets one 
inch long and a pair of woody thorns where the 
leaf stem emerges from the branch. The fragrant 
white flower clusters produce a flat, reddish brown 
fruit pod that remains over the winter months. 

Poisonous part 

The poison is a phytotoxin called "robin," a plant 
lectin (toxalbumin) that interferes with the synthe- 
sis of protein in the small intestine. It is particularly 
prevalent in the inner bark, seeds, and leaves. 

Symptoms 

Appearing within one or more hours, symptoms 
include nausea, vomiting, diarrhea, stupor, weak 
pulse, and gastroenteritis. Poisoning may be fol- 
lowed by shock, convulsions, and death, although 
these are uncommon. 

Treatment 

Gastric lavage; fluid and electrolyte level correc- 
tion; oral administration of magnesium sulfate. 
See also phytotoxins. 



black snake, Australian (Pseudeschis porphyriacus) 

The most common of the poisonous Australian 
snakes, the black snake has a blue-black body with 
a small head and a red belly and is found in marshy 
areas of Austraha. Others in the same group include 
the spotted black snake (P. guttatus) and the mulga 
(P. australis). Note: The Australian black snake 
should not be confused with the American black 
snake, a common — and nonpoisonous — snake. 

Poisonous part 

Its venom is a powerful anticoagulant. 

Symptoms 

Within 15 to 30 minutes symptoms appear: pain, 
swelling, a drop in blood pressure, confusion, slur- 
ring of speech, dilation of the pupils, strabismus 
(abnormal deviation of one eye in relation to the 
other), drooping of the upper eyelid, and muscle 
weakness. The respiratory muscles are affected last. 



and respiratory muscle paralysis is the most com- 
mon cause of death. 

Treatment 

Australian black snake antiserum should be used. 
See also antivenin; snakes, poisonous. 

black widow spider [Other names: button spider 
(South Africa), karakurt (Russia), katipo (New Zea- 
land), malmignatte (Mediterranean).] One of two 

species of poisonous spiders found in the United 
States, the black widow has a globe-shaped, shiny 
black body with a red or orange hourglass-shaped 
mark on its belly. On some spiders, there are several 
triangles or spots instead of the well-known hour- 
glass shape. Male spiders, much smaller than the 
female, may have only a small, reddish dot on their 
belly and are not considered dangerous. Reluctant 
to bite humans, black widows are responsible for 
about three deaths in the United States each year. 
All six species of black widow are venomous, but 
none are usually fatal. 

In the past, however, they were responsible for 
a number of deaths — particularly during swarms, 
recorded in Spain in 1833 and 1841 and in Sardinia 
in 1833 and 1839, when many people were bitten 
and some died. In addition, the Gosiute Indians of 
Utah mixed the venom of the black widow and the 
rattlesnake to coat their arrowheads. 

Black widow spiders build their messy, tangled 
webs under or between rocks, under loose bark, 
around outdoor water faucets, and in woodpiles, 
garages, basements, garbage cans, and sheds. They 
also hide in cushions and under toilet lids, so that 
the most common and deadly bites are on the 
genitals. Although they are found throughout the 
United States and Canada, most inhabit warmer 
regions of the United States. They are also found in 
Mexico, Central America and the Antilles, and the 
western part of South America. 

The brown widow (L. geometrieus) lives in the 
tropics and bears the same markings as the black 
widow, but it rarely bites humans. 

Poisonous part 

The venom of the black widow spider is a neuro- 
toxin that acts on the nerve endings, destroying 



bloodroot 39 



peripheral nerve endings and causing an ascending 
paralysis, usually affecting muscles in the thigh, 
shoulder, and back first. 

Symptoms 

The bite of a black widow is not extremely pain- 
ful and may not be felt at all. There may be shght 
swelling and two tiny puncture marks at the 
wound site, and following the bite there is a dull, 
numbing pain increasing in intensity, peaking in 
one to three hours and continuing up to 48 hours. 
Within 10 to 40 minutes after the bite, the venom 
attacks the nerves, causing abdominal or chest 
muscles to become rigid and flu-hke symptoms 
to appear. At the same time, there is stomach 
pain and muscle spasms in the extremities, along 
with difficulty in breathing and swallowing, chills, 
urinary retention, sweating, convulsions, paraly- 
sis, delirium, nausea, vomiting, drooping eyelids, 
headache, and fever. When death occurs, it is due 
to cardiac failure. Most victims recover without 
serious complications. 

Treatment 

Antivenin is available, but most people can be 
managed without using the equine-derived anti- 
venin. However, it may be needed for elderly 
patients and children, who do not respond to 
more conventional therapy for high blood pres- 
sure, muscle cramps, or respiratory distress, or for 
pregnant women threatening premature labor. 
Apply an ice pack to the bite site and elevate the 
affected limb to heart level. Cleanse the wound 
and treat infection, give a tetanus shot if needed 
and monitor for at least six to eight hours. Muscle 
cramping may be treated with intravenous cal- 
cium or muscle relaxants; pain may be treated 
with morphine. Keep the victim warm and quiet 
and call a physician immediately. 

bleach See alkaline corrosives. 



blister beetle Any of the more than 2,000 species 
of the insect family Meloidae, found throughout 
the Midwest and the eastern United States. These 
beetles secrete an irritating substance called can- 



tharidin, collected from the European species Lytta 
vesicatoria (or Spanish fly). Powdered cantharidin 
is used as a topical skin irritant to remove warts 
and is also intensely irritating to the mucous mem- 
branes. Although Spanish fly has a reputation as 
an aphrodisiac, it is in fact deadly poisonous and 
often fatal. 

Poisonous part 

Blister beetle venom contains large amounts of 
cantharidin, which produces painful blisters and 
reddening when it comes in contact with the 
skin. 

Symptoms 

A large, painful blister with erythema following 
contact with the toxic substance secreted by the 
blister beetle. 

Treatment 

Ice packs to relieve pain; corticosteroid cream is 
helpful. 

See also cantharidin. 



bloodroot (Sanguinaria canadensis) This bitter- 
tasting perennial herb is considered to be very toxic 
and is found from southern Canada to Florida and 
as far west as Texas. It has shiny white poppy- 
like flowers that appear in early spring and when 
squeezed can produce a red juice. Bloodroot extract 
is used commercially as a dental plaque inhibitor. 
Bloodroot is usually found in woodlands and along 
fence rows. 

Poisonous part 

All parts of the plant contain the poison sanguina- 
rine, which reduces the heart's action and muscle 
strength and is a nerve depressant. All parts are 
toxic when eaten; the red sap can cause a painful 
skin rash upon contact. 

Symptoms 

Appearing within one to two hours after ingestion, 
symptoms include violent vomiting, thirst, burning 
and soreness in the throat, heaviness of the chest, 
breathing problems, dilated pupils, faintness, and 
cardiac paralysis resulting in death. 



40 blowfish 



Treatment 

Gastric lavage and symptomatic treatment, 
blowfish See pufferfish. 



boomslang (Dispholidus typus) Found in Africa, 
this is a dangerously venomous snake of the family 
Colubridae, the only rear-fanged colubrid that is 
dangerous to humans. Its venom is lethal in even 
the smallest quantities. 

The boomslang lives in savannas throughout 
sub-Saharan Africa and easily blends into its sur- 
roundings, changing its skin and eye color, which 
makes it difficult to spot. When looking for prey, 
it can lie in a bush or tree, partly extended into 
the air for long periods of time. When provoked, 
the boomslang hisses and inflates its neck, show- 
ing the dark skin between the scales, and then 
strikes. However, it is normally a mild-mannered 
and placid snake that spends all its time in trees. It 
comes in two colors: a brownish gray and a vivid 
green. 

Symptoms 

Pain, swelling, hemorrhage, bleeding from nose 
and mouth, headache, vomiting, collapse, and 
death. The venom of the boomslang is fatal in tiny 
amounts. 

Treatment 

Antivenin is available. 

See also antivenin; snakes, poisonous. 

boric acid This white, crystalline powder is used 
as an antiseptic and, in diluted amounts, to treat 
eye irritations. It is also used as a roach poison, 
food preservative and a buffer in talcum powder. 
The use of boric acid in large amounts on broken 
skin or mucous membranes is toxic. It is no longer 
added to baby powders, and the use of boric acid 
should be strongly discouraged in any products for 
infants. 

While boric acid is fairly safe when used appro- 
priately, it can be extremely dangerous and is toxic 
to all cells — especially those in the kidneys. 



Symptoms 

Primary symptoms are reddened, flaking skin, 
weight loss and hair loss, together with symptoms 
similar to those of toxic shock: fever, vomiting, 
dehydration, anuria, and convulsions. 

Treatment 

For ingestion, immediately perform gastric lavage 
followed by the administration of cathartics. For 
skin contamination, thoroughly wash the skin. 
Symptomatic treatment, including phenobarbital 
or diazepam to control convulsions. 
See also boron. 



boron This natural element is often combined 
with other substances to form compounds called 
borates. Borate compounds include boric acid, salts 
of borates, and boron oxide. Borates are used in 
industry to produce glass, fire retardants, cosmet- 
ics, photographic materials, soaps, cleaners, and 
wood preservatives. It is also used in leather tan- 
ning and high-energy fuel. 

People are exposed to boron in food (primarily 
fruits and vegetables), in cosmetics and laundry 
products, and it is also widely distributed in ground 
water and surface water. Employees of borax min- 
ing and refining plants, as well as facilities where 
boric acid is manufactured, are also exposed to 
boron. 

The Environmental Protection Agency (EPA) 
has determined that exposure to boron in drink- 
ing water at concentrations of 4 parts per million 
for one day or 0.9 parts per million for ten days 
should not cause any adverse effects in children. 
The Agency has also stated that a lifetime exposure 
to I parts per million of boron is not expected to 
cause any adverse effects. 

Symptoms 

Breathing moderate levels of boron in the work- 
place or when using certain products can result in 
productive cough and in irritation to the nose, eyes, 
and throat. Boron toxicity may cause rash, nausea, 
vomiting (may be blue -green in color), diarrhea, 
stomach pain, hypotension, and headache. Fever, 
hyperthermia, seizures, and tremors have also been 
reported. Ingestion of large amounts of boron can 



botulism 41 



cause hair loss and damage to the brain, kidneys, 
liver, intestines, and testes, and can eventually lead 
to death. The acute toxic dose for adults is from 20 
to 60 grams taken in a single dose, but infants have 
died after taking 5 grams, although others have 
survived after being given 9 grams of boric acid. 

Some research indicates that boron increases 
blood levels of estrogen and testosterone as well as 
vitamin D2, calcium, copper, magnesium, and thy- 
roxine (thyroid hormone), and that it reduces blood 
levels of insulin, phosphorus, and calcitonin. 

Treatment 

Symptomatic. 

botanic insecticides Insecticides prepared from 
plant sources. Although many people choose 
"organic" botanic insect controls because they 
somehow seem safer than inorganic chemicals, 
they can still be poisonous. Because they have 
natural sources, botanic insecticides break down 
quickly in the environment and are consumed 
by soil microbes or — in the case of insect dis- 
eases — dissipate when there is no longer anything 
to infect. But they are still poisons; in fact, many 
of these compounds are extremely toxic — some 
more so than their manufactured "chemical" cous- 
ins. Most are deadly to a wide range of insects 
(both the "good" and "bad" insects); and some are 
toxic to birds, other animals, and humans. Botanic 
insecticides include nicotine, pyrethrin/pyrethrum, 
rotenone, neem, ryania. Bacillus thuringiensis 
(Bt), and sabadilla. Because they are derived from 
plants, contact with some of these (such as pyre- 
thrins) can result in an allergic reaction. 

See also Bacillus thuringiensis (Bt); nicotine; 
pyrethrin; pyrethrum; rotenone. 

botulin antitoxin The antidote to poisoning by 
the various strains of Clostridium botulinum (A, B, 
and E) that cause botulism. The antibodies bind 
and inactivate freely circulating botulin toxins, but 
they do not remove toxin that has already bound to 
nerve terminals and will not reverse paralysis that 
has already begun. Therefore, treatment within 
24 hours of the onset of symptoms may shorten 



the course of the poisoning and may prevent total 
paralysis. Botulin antitoxin is not recommended in 
the treatment of infant botulism. 

See also botulin/botulinum toxin; botulism; 
botulism, infant. 



botulin/botulinum toxin The toxin produced by 
the single-celled botulinum bacterium; it is the 
most poisonous substance in the world — 6 million 
times more toxic than rattlesnake venom. When 
ingested, it causes botulism, a form of food poison- 
ing that can cause muscle paralysis and death. 

Despite its deadly reputation, however, botulin 
is also used in small doses to treat various medical 
conditions and for cosmetic reasons. For decades it 
has been administered to manage uncontrollable 
blinking (blepharospasm), misahgned eyes (strabis- 
mus), and cervical dystonia, a neurological disorder 
that causes severe neck and shoulder muscle con- 
tractions. In 2002, botuhn injections (Botox) were 
approved as a temporary treatment to minimize 
frown lines in the face, which it does by weaken- 
ing or paralyzing certain muscles or by blocking 
certain nerves. These effects last about three to four 
months, after which a repeat treatment is needed. 
Side effects may include pain at the injection site, 
flulike symptoms, headache, and upset stomach. 

botulism The most serious type of food poison- 
ing, poisoning by the Clostridium botulinum toxin is 
rare and very deadly — two-thirds of those afflicted 
die, and the rest face a long recovery period. Botu- 
lism is more common in the United States than 
anywhere else in the world owing to the popularity 
here of home canning; there are about 20 cases of 
food-borne botulism poisoning each year. Botulism 
got its name during the 1800s from botulus, the 
Latin word for sausage, in the wake of poisoning 
from contaminated sausages. 

The C. botulinum toxin is found in air, water, and 
food as inactive spores that are harmless — until 
the spores are deprived of oxygen, such as inside 
a sealed can or jar. If conditions are favorable, the 
spores will begin to grow, producing one of the 
most deadly toxins known to humans — 6 million 
times more deadly than cobra venom. 



42 botulism, infant 



Cases of botulism from commercially canned 
food are rare because of strict health standards 
enforced by the Food and Drug Administration, 
and most incidences of botulism occur during 
errors in home canning. Still, it is easy to prevent, 
since botulism is killed when canned food is boiled 
at 212°F for one minute or if the food is first steril- 
ized by pressure cooking at 250°F for 30 minutes. 

While the tightly fitted lids of home-canned food 
will provide the anaerobic environment necessary 
for the growth of botulism toxins, the spores will 
not grow if the food is very acidic, sweet, or salty, 
such as canned fruit juice, jams and jellies, sauer- 
kraut, tomatoes, and heavily salted hams. Canned 
foods that are highly susceptible to contamination 
include green beans, beets, peppers, corn, and 
meat. Although the spores can survive boiling, the 
ideal temperature for their growth is between 78°F 
and 96°F. They can also survive freezing. 

Even though botulism spores are invisible, 
it's possible to tell if food is spoiled by noticing if 
jars have lost their vacuum seal; when the spores 
grow, they give off gas that makes cans and jars 
lose the seal. Jars will burst or cans will swell. Any 
food that is spoiled or whose color or odor doesn't 
seem right inside a home-canned jar or can should 
be thrown away without tasting or even sniffing, 
since botulism can be fatal in extremely small 
amounts. Botulism can also occur if the C. botuli- 
num bacteria in the soil enters the body through 
an open wound. 

Symptoms 

Onset of symptoms may be as soon as three hours 
or as late as 14 days after ingestion, they include 
nausea, vomiting, diarrhea, stomach cramps, weak- 
ness, blurred vision, headache, difficulty in swal- 
lowing, slurred speech, drooping eyehds, dilated 
pupils, and paralysis progressing to the respiratory 
muscles. The earlier the onset of symptoms, the 
more severe the reaction. Symptoms generally 
last between three and six days; death occurs in 
about 70 percent of untreated cases, usually from 
suffocation as a result of respiratory muscle paraly- 
sis. In infants, symptoms may go unrecognized 
by parents for some time until the poisoning has 
reached a critical stage. Infant botulism symptoms 
include constipation, facial muscle flaccidity, suck- 



ing problems, irritability, lethargy, and floppy baby 
syndrome. 

Treatment 

Prompt administration of the antitoxin (type ABE 
botulinus) lowers the risk of death to 25 percent. 
The Centers for Disease Control and Prevention 
in Atlanta, Georgia, is the only agency with the 
antitoxin, and it makes the decision to treat. Local 
health departments should be called first for this 
information. Emesis is indicated immediately fol- 
lowing ingestion of food known to contain botu- 
lism toxin. But since emesis may not be complete 
and the disease can occur with a small amount of 
toxin, botulism may still develop. Patients with 
symptoms should not have lavage or an emetic. 
Enemas may be necessary. Patients are usually put 
on a respirator to ease breathing difficulties. In 
infant botulism, if symptoms are present, it is often 
too late to administer antitoxin, since the damage 
probably has already been done by the toxin. How- 
ever, it is still possible to try. 

See also botulin antitoxin; botulin/botulinum 
toxin; botulism, infant. 

botulism, infant Unlike botulism in adults, which 
occurs after eating contaminated food, infant botu- 
lism is caused by the production of toxin produced 
by C. botulinum in the infant's intestinal tract. While 
it is believed that adults, children, and infants con- 
sume C. botulinum spores on a regular basis — since 
they are present in a wide variety of foods, house 
dust, etc. — for some reason the intestinal tracts 
of some infants under age one are susceptible to 
the spores. In particular, there appears to be a 
link between spores and honey; infants have died 
from eating honey contaminated with the spores, 
and for this reason, children under age one should 
never be fed honey. 

Since researchers have not yet discovered why 
some infants appear to be susceptible to the botu- 
lism spores, parents are advised to keep rooms 
dust free and not to feed honey or corn syrups. 
Commercially prepared foods that are sterilized 
and contain low add are botulism free. Research 
also suggests that mother's milk may also pro- 
vide some immunological protection against infant 



bronchial tube relaxers 43 



botulism, although this has not yet been proven. A 
human-derived antitoxin is now available to treat 
infant botuhsm. Called Botulism Immune Globulin 
Intravenous (BIG-IV), it should be given as soon 
as possible after botulism is identified. Results of 
a five-year, double-blind, placebo-controlled trial 
found that infants who were treated with BIG-IV, 
when compared with controls, had a significant 
mean reduction in the length of the hospital stay, 
from 5.7 weeks to 2.6 weeks, as well as a reduced 
mean duration of stay in intensive care by 3.2 
weeks, reduced use of mechanical ventilation by 
2.6 weeks, and reduced use of tube or intravenous 
feeding by 6.4 weeks. Hospital costs were also 
significantly reduced. No adverse side effects were 
noted associated with use of BIG-IV. 

See also botulin antitoxin; botulin/ Botulinum 
toxin; botulism. 

brewer's yeast Once an antidote for thalhum 
ingestion (found in depilatories and rat poison); it 
is no longer routinely used. 
See also thallium. 



bromates (potassium bromate) A corrosive poi- 
son once widely used (between the 1940s and the 
1970s) in the neutralizer solutions of home per- 
manent kits. While less toxic substances have now 
been substituted for products offered to consumers 
in the home, poisonings do still occur from products 
used by professionals. Bromates may still be found 
in commercial bakeries (bromate salts improve 
bread texture) and in the production of some types 
of explosives. They have been banned by many 
countries, including Canada and England. 

Poisonous part 

Bromate is usually found as a 3 percent solution 
with water and must be taken orally to be toxic. 
It becomes poisonous when the hydrochloric acid 
in the stomach turns the potassium bromate into 
hydrogen bromate, an irritating acid. 

Symptoms 

Within five to 20 minutes after ingestion, bromates 
can cause vomiting, collapse, diarrhea, abdominal 



pain, lethargy, deafness, coma, convulsions, low 
blood pressure, kidney damage, and a skin rash. 

Treatment 

Gastric lavage or an enema, with solutions contain- 
ing sodium bicarbonate; sodium thiosulfate is given 
intravenously as an antidote. 

bromide This former sedative was once found in 
over-the-counter products ranging from Bromo- 
Seltzer and Dr. Miles' Nervine, but today it is rarely 
used because of its potential toxicity. It can be 
found occasionally in well water and in some bro- 
mide-containing hydrocarbons. Because bromide 
affects not just the skin and stomach but the brain, 
and thus can cause a variety of aberrant behaviors, 
bromide exposure in the past was responsible for a 
number of admissions to psychiatric hospitals. 

Symptoms 

Nausea, vomiting, gastric irritation, lethargy, con- 
fusion, hallucinations, psychosis, weakness, stupor, 
coma, anorexia, constipation, and rashes. 

Treatment 

There is no specific antidote, but because bromide 
is excreted entirely by the kidneys, intravenous 
administration of sodium chloride will enhance 
elimination. Induce vomiting or perform gastric 
lavage if ingestion has been recent. 

bronchial tube relaxers Also called bronchial 
tube dilators, these drugs are used to alleviate 
asthma, bronchitis, and emphysema and to relieve 
spasms and tightness in the chest. They can be fatal 
if used in excessive amounts. Bronchial tube dila- 
tors also cause serious side effects if taken with or 
soon after another bronchial tube relaxer or decon- 
gestant pills or liquid. These drugs are dangerous 
when taken with antihypertensives, epinephrine 
and lithium. If taken with beta blockers, the effect 
of both drugs is diminished. 

Symptoms 

In large doses, bronchial fluid builds up and causes 
inflammation, pounding heartbeat, dizziness. 



44 brown recluse spider 



nervousness, bad taste in the mouth, dry mouth, 
headache, insomnia, anxiety, tension, blood pres- 
sure changes, flushing, sweating, angina, and arm 
pain. Overdoses can cause convulsions, low potas- 
sium levels, hallucinations, serious breathing prob- 
lems, fever, chills, vomiting, clammy skin, spike in 
blood pressure, and stroke. 

Treatment 

Administer oxygen and treat symptoms as needed. 

brown recluse spider (Loxosceles reclusa) [Other 
names: fiddleback or violin spider.] The brown 
recluse is one of two species of poisonous spiders 
found in the United States and is by far the most 
dangerous of the spider family — ounce for ounce, 
its venom is more deadly than that of many poi- 
sonous snakes. 

Native to Central and South America, the 
brown recluse is thought to have been inadver- 
tently imported to the United States in crates of 
fruit and vegetables within the last 50 years. Since 
then, it has been making its way steadily north and 
westward and is now found ranging to Texas and 
Arkansas and as far north as Massachusetts. 

Its brown or fawn-colored body is about a half 
inch long and has a dark, violin-shaped mark 
on its back. Although brown recluse spiders are 
sometimes found outdoors, most live in houses, 
spinning their webs in dark areas inside homes or 
outbuildings. They get their name from their habit 
of hiding in closets, dresser drawers, the folds of 
clothing, garages, attics, and sheds. Brown recluse 
spiders are not aggressive and will try to escape, 
not attack; but if trapped, they will bite. The venom 
of females is more deadly than that of males. 

Symptoms 

The bite of a brown recluse causes little pain, but 
within two to eight hours the pain will be severe 
and the area of the bite will become red. Any place 
on the skin the spider has bitten will necrose and 
die. Brown recluse venom contains a substance 
that is very destructive to tissue and causes a large, 
spreading sore that eventually turns into a blister, 
becoming dark and hard within four days. In some 
cases, this sore becomes star shaped and deep 



purple and within two weeks forms an open ulcer, 
although the venom does not necessarily kill. As 
this ulcer heals, it often becomes infected; in a very 
small percentage of victims the ulcer does not heal 
for an extremely long time. 

The bite can also cause a range of systemic reac- 
tions, including fever, chills, weakness, nausea, 
vomiting, joint pain, and sometimes a generalized 
rash or reddish spots. Death, when it does come, 
usually occurs within the first 48 hours as a result 
of renal failure because of blood coagulation. 

Treatment 

There is no specific antivenin, although antivenin 
for other species of brown spiders of South America 
should give protection. Since this antivenin contains 
norepinephrine, administration of phentolamine 
may help head off swelling and necrosis. Antihista- 
mines, muscle relaxants, and adrenocortical steroids 
may provide some relief. Exchange transfusion may 
be attempted. Immediate excision of the bite area 
may be the only way to prevent the massive necro- 
sis caused by the brown recluse venom, although 
not all experts agree on this treatment. Most physi- 
cians will not touch the lesion until all destruction 
has been done, sometimes as long as 40 weeks after 
the bite. Skin grafts may be necessary to heal the 
ulcer. If the bite of a brown recluse is suspected, a 
physician should be called at once. 

See also antivenin; spider, poisonous. 



brown snake (Demansia textilis) Found in Aus- 
tralia, the brown snake includes any of several 
species named for their primary color, ranging from 
light brown to dark green. This slender member 
of the cobra family can be about 7 feet long and 
is extremely bad tempered and poisonous. When 
threatened, it will rear and strike repeatedly. It is 
responsible for more deaths in Australia than any 
other snake. Brown snakes found in the West- 
ern Hemisphere are sometimes also called grass 
snakes, ranging from Canada to Honduras, and are 
harmless. 

Symptoms 

Symptoms can take up to 12 hours to appear and 
include abdominal pain, staggering gait, problems 



bushmaster 45 



in swallowing, stiff jaws, respiratory distress, coma, 
cardiac failure, and death. 

Treatment 

Copperhead antivenin is used for this snakebite. 
See also antivenin; cobra; snakes, poisonous. 

brown spider See brown recluse spider. 

bryony (Bryonia dioica, B. alba or B. cretica) Also 
called the devil's turnip or British mandrake, 
bryony is considered to be very toxic (fewer than 
40 berries will kill an adult). A common climb- 
ing plant in public gardens with pretty red berries 
and black and yellow seeds, bryony blooms in the 
summer and is found in England, Wales, and other 
northern countries. The entire plant has a foul- 
smelling milky juice, and its fleshy white roots can 
be mistaken for turnips or parsnips. When the ber- 
ries are distilled, the resulting beverage can cause 
abortions. Medically, it can be used as a diuretic. 

Poisonous part 

Roots and berries contain the poisons glycoside, 
bryonin, and bryonidin. 

Symptoms 

Within several hours after ingestion, victims expe- 
rience burning mouth, nausea, vomiting, diarrhea, 
convulsions, paralysis, and coma; death follows 
because of respiratory arrest. The juice can also 
irritate the skin and cause a rash. 

Treatment 

Perform gastric lavage, while keeping the victim 
warm and quiet. Replace fluids and monitor electro- 
lyte levels, and provide pain medication as needed. 
See also glycoside. 



buckeye (Aesculus) [Other names: conquerors, 
horse chestnut, fish poison.] These trees — con- 
sisting of about 13 species — have white, pink, 
yellow, and red clusters of flowers and compound 
leaves. The seed pod is leathery, with glossy brown 
seeds bearing a brown scar. The trees are found in 



the central and eastern temperate zones to the Gulf 
Coast and California and in parts of Canada. 

Poisonous part 

Flowers, nuts, sprouts, and twigs are toxic and 
contain a mixture of cytotoxic saponins known as 
aescin. 

Symptoms 

Because the saponins are not well absorbed, poison- 
ing is generally not fatal unless as a result of frequent 
exposure. In addition, the unpleasant taste usually 
prohibits ingestion in large enough quantities to kill. 
Generally, symptoms are limited to severe gastroen- 
teritis, inflammation of mucous membranes, depres- 
sion, weakness, and paralysis. However, there have 
been reports of fatalities among children. 

Treatment 

Gastric lavage, general treatment for gastroen- 
teritis, with fluid and electrolyte replacement and 
administration of oral magnesium sulfate. 
See also saponin. 



bushmaster (Lachesis muta) One of the larger and 
most dangerous South American pit vipers is the 
bushmaster, which is found in tropical forests from 
Costa Rica to the Amazon Basin. The longest ven- 
omous snake in the New World (it can grow up to 
12 feet long), the bushmaster can be either tan or 
pink with dark diamond markings, and while this 
snake is rarely seen, its bite is potentially lethal. 

The bushmaster is the only American pit viper 
that lays eggs. 

Symptoms 

Within a very short time, victims begin bleeding 
from the gums, nose, and eyes and experience 
chills, fever, sweating, falling blood pressure, con- 
vulsions, and death. In cases of a severe bite, the 
victim will also experience swelling above the 
elbows or knees within two hours. 

Treatment 

Death from heart failure is unavoidable unless 
antivenin is given quickly. 

See also antivenin; pit vipers; snakes, poisonous. 



46 buttercup 



buttercup (Ranunculus) [Other names: bassinet, 
blister flower, butter-cress, butter daisy, butter- 
flower, crowfoot, devil's claws, figwort, goldballs, 
goldweed, horse gold, hunger weed, lesser celandine, 
pilewort, ram's claws, St. Anthony's turnip, sitfast, 
spearwort, starve-acre, water crowfoot.] Annual 
or perennial herbs that grow in wet, moist, or 
swampy places throughout the United States and 
Canada. They range in height from a few inches to 
3 feet tall, with yellow, red, or white flowers. 

Poisonous part 

The sap and roots are toxic and contain protoane- 
monin, a direct irritant and vesicant of the skin and 
mucous membranes. 



Symptoms 

After ingestion, symptoms include severe pain, 
swelling, and blisters in the mouth, followed by 
bloody diarrhea and painful abdominal cramps. 
The toxin, which affects the central nervous sys- 
tem, also causes systemic symptoms including diz- 
ziness and sometimes convulsions. 

Treatment 

Because of the intense pain following ingestion, 
large amounts of this plant are generally not eaten. 
If this is the case, gastric lavage is recommended 
followed by the administration of demulcents 
(such as milk); give plenty of fluids and monitor 
kidney function. 



c 



cadmium Found in sulfide ores (togetiier witli 
zinc and lead), cadmium is used in electroplating, 
as a pigment and stabilizer in plastics, in solder- 
ing and welding and in nickel-cadmium batteries. 
Solder made of cadmium used for water pipes, and 
cadmium pigments in pottery, can contaminate 
water and acidic food. 

Symptoms 

Cadmium fumes and dust are at least 60 times 
more toxic than other forms, causing chemical 
pneumonitis and pulmonary edema and hemor- 
rhage, in addition to coughs, wheezing, head- 
ache, and fever. Symptoms appear within f2 to 
24 hours after inhalation. Ingested cadmium, 
on the other hand, affects the gastrointestinal 
tract and the kidneys, causing nausea, vomiting, 
cramps, diarrhea, and death as a result of shock 
or acute kidney failure. The kidney damage is 
irreversible. 

Treatment 

There is no evidence that chelation therapy is 
effective. In cases of inhalation poisoning: Monitor 
blood and general condition; remove the victim 
from exposure and give supplemental oxygen if 
necessary. For ingestion: Treat fluid loss; perform 
gastric lavage but do not induce vomiting because 
cadmium salts are an irritant; and administer acti- 
vated charcoal (but do not give cathartics in the 
presence of diarrhea). 

caffeine This alkaloid is one of the most widely 
consumed drugs in the United States and is con- 
tained in a wide variety of products, including cof- 
fee, chocolate, medications, and over-the-counter 
stimulants. 



In one recent study, about 30 percent of Ameri- 
cans said they drank between five and 10 cups of 
coffee a day, resulting in a daily dose of 500 to 600 
milligrams of caffeine daily. 

Caffeine can be found naturally in kola nuts, 
cocoa beans, tea leaves, and coffee beans. This 
white, odorless, crystalline powder was first 
extracted from plants in 1820. Caffeine is quickly 
absorbed orally, rectally, and through the skin and 
is rapidly metabolized and excreted. At one time, it 
was often combined with aspirin and phenacetin in 
a wide range of prescription and over-the-counter 
medications, and it is still included today in many 
analgesics, stimulants, and cold preparations avail- 
able without a prescription. 

It is believed that caffeine affects the synthesis 
and release of catecholamines (especially the stress 
hormone norepinephrine), and after ingestion, it 
quickly disperses throughout all organ systems, 
crossing both the blood-brain barrier and the 
placenta. At high doses, it affects blood vessels, 
breathing, the brain, and the spinal cord. 

In newborns, however, the metabolism of 
caffeine is markedly delayed, which contributes 
to caffeine toxicity in infants exposed to the 
substance. 

Symptoms 

Caffeine toxicity can be chronic or acute, but 
despite its extreme popularity, few deaths have 
been recorded. The acute lethal dose of caffeine in 
adults may be as low as 6 grams, although the dose 
is much lower for children. One gram can cause 
symptoms of toxicity. 

Chronic "caffeinism" is caused by constantly 
consuming products containing caffeine, such as 
colas and chocolates. The effects might include 
headache, indigestion, insomnia, restlessness. 



47 



48 calcium 



AMOUNTS OF CAFFEINE IN COMMON PRODUCTS 



Source 


Amount* 


Dose 


Beverages 






Brewed coffee 


85-120 mg 


cup 


Instant coffee 


60-1 00 m 


cup 


Cola** 


25-60 mg 


glass 


Tea 


30-75 mg 


cup 


Cocoa 


6-42 mg 


cup 


Decaffeinated coffee 


2-6 mg 


cup 


Medications 






Migraine drugs 


50-1 00 mg/dose 




Analgesics 


1 5-40 mg/dose 




Cough/cold 


1 5-1 25 mg/dose 




Over-the-counter stimulants 


65-250 mg/dose 





* Approximation based on range gathered from several sources 
** Caffeine-containing colas only 



nervousness, confusion, tremors, constipation, 
fever, and sensory disturbances. 

Toxic symptoms can appear in adults after one 
gram of oral caffeine. Victims of caffeine toxicity 
often complain of irregular heartbeat and nervous- 
ness, together with sleeplessness, excitement, and 
mild delirium. In severe cases of overdose, symp- 
toms include loss of consciousness, rapid heartbeat, 
irregular heart rhythms, seizures, and caffeine- 
induced psychosis. A number of deaths have report- 
edly occurred following caffeine-induced seizures. 
There have also been cases in which caffeine has 
worsened the symptoms of persons already suffer- 
ing from schizophrenia or manic-depression. The 
most widespread and chronic symptom of caffeine 
is a severe headache upon withdrawal, although 
the reason behind this is not known. 

Treatment 

Gastric lavage, with supportive and symptomatic 
treatment including withholding further caffeine. 
To control seizures, diazepam and phenobarbital 
can be administered. Cardiac evaluation is essen- 
tial, as death is most commonly due to arrhythmia. 
Specific treatment may be necessary. 

calcium Necessary for the normal function of a 
wide variety of enzymes and organ systems in the 
body, calcium is used in the treatment of poisoning 



by fluoride, oxalate, phosphate, or the intrave- 
nous anticoagulant citrate. It is also helpful in the 
treatment of muscle cramping or rigidity following 
black widow spider bites. Calcium overdose can 
cause kidney stones, constipation, and calcium 
deposits in the body. Recommended upper limits is 
2,500 milligrams a day. 

See also black widow spider; fluoride; oxa- 
lates; PHOSPHATE ESTERS. 

calcium EDTA This chelating agent is used in 
the treatment of acute and chronic lead poison- 
ing and may also be helpful to treat poisoning 
with manganese, zinc, chromium, nickel, or heavy 
radioisotopes. It is not effective in the treatment of 
mercury, gold, or arsenic poisoning. 

See also arsenic; lead poisoning; mercury. 

calcium oxalate See oxalates. 



California mussel (Mytilus californianus) These 
mollusks become poisonous to eat because of feeding 
on toxic one-celled animals called dinoflagellates. 

See also dinoflagellate; paralytic shellfish 
poisoning; shellfish poisoning. 

camphor This respiratory aid and mild local 
anesthetic is found in mothballs and liniments; the 
related compound camphorated oil (a 20 percent 
solution of camphor in oil) is highly toxic but was 
banned by the Food and Drug Administration in 
1982. Both the ingestion of camphor and the pro- 
longed inhalation of camphor vapors can be toxic. 
Because of its strong medicinal odor, camphor is 
included in a large number of over-the-counter 
products. Camphor is rated as very toxic, with a 
lethal dose of 50 to 500 milligrams per kilogram. 
According to the Food and Drug Administration, 
in 1979 alone there were 768 cases of camphor 
poisoning and more than 20 fatalities. All of these 
fatalities were the result of either a child acciden- 
tally ingesting a product not labeled as toxic that 
was intended for topical use, or the accidental sub- 
stitution of a camphor-containing medicine instead 



cantharidin 49 



of the proper drug (most commonly, camphor for 
castor oil or cod liver oil). 

Symptoms 

Appearing within 1 5 to 60 minutes after ingestion 
or prolonged vapor inhalation, symptoms include 
headache, excitement, a feeling of warmth, clammy 
skin, weak pulse, nausea, vomiting, burning in the 
mouth and throat, and delirium. Camphor can also 
be smelled on the breath. Twitching and muscle 
spasms may be followed by convulsions and circu- 
latory failure. 

Treatment 

Gastric lavage followed by administration of acti- 
vated charcoal via tube. Vomiting is not induced 
because of the danger of seizures. Valium may be 
used to control convulsions; hemodialysis may 
help eliminate the drug from the body. 

campylobacteriosis Campylobacter was first recog- 
nized in the 1970s as a cause of campylobacterio- 
sis, the so-called traveler's diarrhea. Linked to raw 
and undercooked poultry, unpasteurized milk, and 
untreated water, this common foodborne illness 
causes an estimated 4 million infections and 1,000 
deaths every year. While the illness can be uncom- 
fortable and even disabling, deaths occur primarily 
among those with impaired immune systems, the 
very young, or the very old. In one of the best- 
known outbreaks during the 1980s, more than 3,000 
residents in Bennington, Vermont, became ill with 
diarrhea when their town's water supply was con- 
taminated with the rod-shaped bacterium. The dis- 
ease may also spread throughout child-care centers. 

The most common source of infection is con- 
taminated poultry (one-third to half of all raw 
chicken on the market is contaminated). Consum- 
ers get sick when they eat undercooked chicken, or 
when the organisms are transferred from the raw 
meat or raw meat drippings to the mouth. It also 
can survive in undercooked lamb, beef, or pork, in 
water, and in raw milk. 

Symptoms 

Symptoms begin between two to 10 days and may 
last up to 10 days; they include fever, headache. 



and muscle pain followed by sometimes-bloody 
diarrhea, abdominal pain and nausea, fatigue and 
body aches. The infection can be fatal. The Centers 
for Disease Control and Prevention estimates 100 
people die of the disease each year. 

Diagnosis 

The infection is diagnosed by culturing a stool 
sample. 

Treatment 

Unless antibiotics are taken at the very beginning of 
the illness they won't alleviate symptoms, although 
they will shorten the infectious period. Without 
treatment, stool is infectious for several weeks, but 
three days of antibiotics will eliminate the bacteria. 
For mild cases, rest and fluids should be sufficient. 
Young children are usually given antibiotics (usu- 
ally erythromycin) as a way of reducing the risk of 
passing the infection on to other children. 

Complications 

Occasionally infection may provoke meningitis, uri- 
nary tract infections, reactive arthritis, or a paralyzing 
neurologic illness called Guillain-Barre syndrome. 

Prevention 

Avoid unpasteurized milk or untreated water from 
mountain streams or lakes. 

cantharidin A powder obtained from the bhster 
beetle, cantharidin is used to remove warts and 
is extremely irritating to the mucous membranes. 
Nicknamed "Spanish fly," it is popularly believed to 
be an aphrodisiac; it is in fact a deadly poison that 
is responsible for many fatalities. When ingested, 
Spanish fly is highly toxic. 

Symptoms 

Ingestion of Spanish fly causes burning in the throat 
and sloughing of the upper gastrointestinal tract. 
Kidney failure can occur, and death often follows. 

Treatment 

Dilute with four to eight ounces of water. Do not 
induce emesis. Treatment is also supportive; hemo- 
dialysis may be necessary if the kidneys fail, and 



50 cantil snake 



treatment of the throat injury is similar to that for 
lye ingestion. Also, treat gastrointestinal bleeding. 
See also blister beetle. 



cantil snake (Agkistrodon bilineatus) Also called a 
Mexican moccasin, this pit viper is a brightly colored 
and extremely dangerous snake found in the low 
regions of the Rio Grande all the way to Nicaragua. 
Related to the cottonmouth (or water moccasin), 
this snake has a yellow or red tail that contrasts with 
the dull appearance of the rest of the body. 

Pit vipers seem to be extremely highly evolved 
for capturing, killing, and eating fairly large, warm- 
blooded prey, with retractable hollow fangs in the 
front of the upper jaw. The fangs can be folded back 
and then positioned forward as the mouth opens 
to strike. The pit viper's name comes from the 
heat-sensitive pits located on each side of the head 
between the nostril and the eye, which are used to 
locate its prey. 

Seriousness of the bite depends on a wide vari- 
ety of variables, including the snake's size (usually 
the larger, the more venomous) and whether the 
snake is hungry or alert. The angle of the bite and 
its depth and length also affect the seriousness 
of the bite. In addition, the size of the victim can 
be important (children and infants are at greater 
risk), and the health of the victim at the time of 
the bite will also affect the outcome. Persons with 
diabetes, hypertension, or blood coagulation prob- 
lems and the elderly are particularly sensitive to 
snake venom, and menstruating women may bleed 
excessively following the bite of a pit viper. Sev- 
eral cases of miscarriage have been reported when 
pregnant women have been bitten. 

Finally, the location of the bite itself is crucial 
to its seriousness; venomous snake bites on the 
head and trunk are twice as serious as those on the 
extremities, and bites on the arms are more serious 
than those on the legs. 

Poisonous part 

The venom of the pit vipers is a mixture of pro- 
teins that acts on a victim's blood. Even snakes 
that appear to be dead by the side of the road have 
been reported to bite. The size of the snake can 
give an idea of its potential dangerousness and can 



be judged by the distance between the fang marks. 
Fang marks less than 8 mm would be a small 
snake; between 8 and 12 mm indicates a medium- 
size snake, and more than 12 mm suggests a large 
venomous snake. Even snakes that have been 
"defanged" can be dangerous, since all snakes grow 
new fangs from time to time. 

Symptoms 

Swelling, internal bleeding, changes in red blood 
cells; central nervous system symptoms sometimes 
include convulsions, psychotic behavior, muscle 
weakness, and paralysis. In addition, there are gen- 
eral systemic symptoms of fever, nausea, vomiting, 
diarrhea, pain, and restlessness. Tachycardia and 
bradycardia can develop, and kidney failure has 
been reported. 

Treatment 

Within the first 30 to 45 minutes after the bite of 
a pit viper, apply a venous tourniquet a few inches 
above the bite, loosening it every 15 to 30 min- 
utes and reapplying it above the level of progres- 
sive swelling. Keep the victim quiet, lying down 
to decrease metabolic activity (which affects the 
spread of the venom). The wound area (especially 
if it is an arm or leg) should be kept lower than 
the heart. Within 30 minutes, trained individu- 
als can incise the wound area and apply suction. 
Antivenin is available but should be administered 
within four hours; antivenin is rarely helpful if 
given more than 12 hours after the bite. Tetanus 
prophylaxis is advisable; other treatment might 
include blood transfusions, intravenous fluids, 
treatment for convulsions, and antihistamines to 
control itching. In addition, broad-spectrum anti- 
biotics may be administered, since snakebites are 
notorious for becoming infected. If antivenin has 
not been administered (or was given hours after 
the bite), sloughing of the skin around the bite is 
common. Some individuals may be sensitive to the 
antivenin, so skin testing is advised. 

While certain anecdotal reports in the popular 
press have reported that some individuals become 
immunized after many bites of the pit viper, scien- 
tifically controlled attempts to develop immunity 
in human beings have failed. 

See also antivenin; pit viper; snakes, poisonous. 



carbon monoxide 51 



carbamate A group of synthetic pesticides made 
up of carbon, fiydrogen, oxygen, and nitrogen. 
They include carbaryl, chlorpropham, carbofuran, 
aldicarb, pirimicarb, bufencarb, isolan, maneb, pro- 
poxur, thiram, Zectran, zineb, and ziram. 

Symptoms 

Generally, poisoning signs and symptoms may 
include headache, dizziness, nausea, diarrhea, 
blurry vision, constricted pupils, slowed heart rate, 
excessive sweating and salivation, inability to walk, 
chest discomfort, muscle twitching, incontinence, 
unconsciousness, and seizures. 

Treatment 

Atropine is the antidote for most carbamate 
poisonings. 

See also carbaryl; organophosphate insecti- 
cides. 



carbaryl (Sevin) This derivative of carbamic acid 
(H2N-COOH) is used as an herbicide, insecticide, 
and medicinal agent and is one of the carbamates, 
a relatively new class of contact insecticides that 
supplement the organophosphates. 

Symptoms 

Carbaryl poisoning resembles parathion intoxica- 
tion, although it is much less toxic. Symptoms 
include nausea, vomiting, abdominal cramps, diar- 
rhea, excess salivation, sweating, lassitude, weak- 
ness, tightness in the chest, blurring of vision, eye 
pain, loss of muscle coordination, slurred speech, 
muscle twitches, breathing problems, blue skin, 
incontinence, convulsions, and coma. Death occurs 
from respiratory arrest and paralysis of the respi- 
ratory muscles. It is an eye and skin irritant and 
does not accumulate in the tissues. It is poisonous 
through ingestion or skin absorption. 

Treatment 

Give atropine immediately; some reports suggest 
atropine is dangerous in the presence of anoxia 
(loss of oxygen); correct cyanosis (blueness of skin) 
before giving atropine. Give oxygen, artificial respi- 
ration as needed. Perform gastric lavage or admin- 
ister syrup of ipecac if vomiting is not prompt. 



Wash contaminated skin with soap and water (or 
95 percent ethyl alcohol). Irrigate affected eyes 
with water or saline. Administer isotonic saline to 
counteract dehydration and electrolyte imbalance. 
See also carbamate; organophosphate 

INSECTICIDES. 



carbolic acid See phenol. 



carbon monoxide A colorless, odorless, poison- 
ous gas that is produced by the incomplete combus- 
tion of sohd, liquid, and gaseous fuels. Appliances 
fueled with gas, oil, kerosene, or wood may pro- 
duce carbon dioxide. If these appliances aren't 
installed, maintained, and used properly, carbon 
monoxide may accumulate to dangerous levels. 

Carbon monoxide is also found in the exhaust 
of internal-combustion engines, including car 
engines. Common sources include gas cooking 
ranges, hot water heaters and dryers, wood- or 
coal-burning stoves and fireplaces, oil burners, and 
kerosene heaters. Gas water heaters and dryers and 
oil burners must have stacks that direct the car- 
bon monoxide outside. Wood-burning stoves and 
fireplaces must have chimneys that vent the gas 
outside. Unvented kerosene heaters spread carbon 
monoxide gas indoors; therefore, a window must 
always be open slightly when you use a kerosene 
heater. Cooking with a charcoal grill in an enclosed 
area also releases carbon monoxide; for this reason, 
such grills should never be used indoors. 

More than 20,000 people in the United States 
are treated yearly in hospital emergency rooms 
for carbon monoxide poisoning; this number is 
believed to be low, since many people mistake 
the symptoms for the flu or are misdiagnosed and 
never get treated. 

Symptoms 

Breathing carbon monoxide causes headaches, 
dizziness, weakness, sleepiness, nausea, vomiting, 
confusion, and disorientation. At very high levels, 
the level of the gas in the blood rises, leaving the 
patient confused and clumsy. Loss of consciousness 
and death soon follow. Symptoms are particu- 
larly dangerous because the effects often are not 



52 carbon tetrachloride 



recognized, since the gas is odorless and some of 
the symptoms are similar to the flu or other com- 
mon illnesses. Breathing low levels of the chemical 
can cause fatigue and increase chest pain in people 
with chronic heart disease; indeed, it has some- 
times caused fatal heart attacks. 

Some people are particularly susceptible to car- 
bon monoxide, including unborn babies, infants, 
and people with anemia or a history of heart 
disease. 

Treatment 

It's essential to get the victim into fresh air right 
away, and then call for help. If the victim isn't 
breathing (or is breathing irregularly), perform 
artificial respiration. Keep the victim warm and 
quiet to prevent shock. Medical personnel can give 
oxygen (often with 5 percent carbon dioxide and 
sometimes under pressure). A physician should be 
consulted to check for long-term effects, even if the 
victim seems to have recovered. 

Prevention 

Dangerous levels of carbon monoxide can be pre- 
vented by proper apphance use, maintenance, and 
installation. A qualified service technician should 
check a home's central and room heating appli- 
ances (including water heaters and gas dryers) each 
year. The technician should look at the electrical 
and mechanical components of appliances, such as 
thermostat controls and automatic safety devices. 
In addition, 

• chimneys and flues should be checked for block- 
ages, corrosion, and loose connections; 

• individual appliances should be serviced regularly; 

• kerosene and gas space heaters (vented and 
unvented) should be cleaned and inspected to 
make sure they operate properly; 

• new appliances should be installed and vented 
properly; 

• adequate combustion air should be provided to 
assure complete combustion; 

• the room where an unvented gas or kerosene 
space heater is used should be well ventilated, 
and doors leading to another room should be 
open to insure proper ventilation; and 



• an unvented combustion heater should never be 
used overnight or in a room where someone is 
sleeping. 

Although carbon monoxide can't be seen or 
smelled, there are tangible signs that might indi- 
cate a problem: visible rust or stains on vents and 
chimneys, apphances that make unusual sounds or 
smells, or an appliance that keeps shutting off. 

One of the best ways to prevent carbon monox- 
ide poisoning is to install carbon monoxide detec- 
tors that meet the requirements of Underwriters 
Laboratories (UL) standard 2034. Detectors that 
meet the UL standard measure both high carbon 
monoxide concentrations over short periods of 
time and low concentrations over long periods of 
time. Detectors sound an alarm before the level of 
carbon monoxide in a person's blood becomes dan- 
gerous. Detectors that meet the UL 2034 standard 
currently cost between $25 and $100. 

Since carbon monoxide gases move evenly and 
fairly quickly throughout the house, a CO detector 
should be installed on the wall or ceiling in sleep- 
ing areas but outside individual bedrooms. 

In addition, there are inexpensive cardboard or 
plastic detectors that change color and do not sound 
an alarm and have a limited useful life, since they 
require someone to look at the device to determine 
if the gas is present. Since carbon monoxide can 
build up rapidly while a family sleeps, these devices 
would not sound an alarm to awaken people. 

carbon tetrachloride A colorless, volatile liquid 
with a characteristic odor, this once-common house- 
hold solvent is used to clean metals, in dry cleaning, 
and to remove oil, grease, wax, and paint. An ingre- 
dient in fire extinguishers and insecticide sprays, it 
is also used in the manufacture of Freon propellants 
and refrigerants. Consumers can no longer buy car- 
bon tetrachloride; it is available only for industrial or 
commercial use. This dangerous chemical can cause 
liver and kidney damage if inhaled or drunk. 

Symptoms 

Breathing these solvent fumes can cause headache, 
eye irritation, dizziness, visual disturbances, and 
nausea. In extreme cases, inhaling these fumes 



cassava 53 



can be fatal. If this cfiemical is drunk, symptoms 
include headache, nausea, pain in the abdomen, 
and convulsions. 

Treatment 

Victim should vomit unless unconscious or hav- 
ing convulsions. If fumes were inhaled, the victim 
should be taken into fresh air and given artificial 
respiration if necessary. Skin contamination should 
be treated with running water for at least 1 5 min- 
utes. Drinking large amounts of this substance has 
been reported to be fatal in 90 percent of cases, but 
with early intervention prognosis is good. 

carbutol See barbiturates. 



cardiac glycosides One of the toxic glycosides 
in the plant kingdom that affect the heart, cardiac 
glycosides remain one of the major therapies for 
congestive heart failure. There are more than 400 
different types, but the most common is digitalis, 
which is found in the foxglove (Digitalis purpurea) 
and other "digitoxins" (similar to digitahs) found in 
Nerium oleander and the lily family. 

Most cardiac glycosides come from the figwort, 
lily, and dogbane families. In therapeutic amounts, 
they will act directly on the heart to increase the 
force of contractions and decrease the heartbeat — 
but no one knows how. 

Symptoms 

Overdoses produce nausea, dizziness, blurred 
vision, and diarrhea. It is suspected that there is 
a relationship between the cardiac glycosides and 
plant toxicity. Poisonous plants containing cardiac 
glycosides include pheasant's-eye, dogbane, lily of 
the valley, foxglove, and oleander. 

Treatment 

Treatment may include administration of activated 
charcoal, gastric lavage, an electrocardiogram, and 
blood tests to check digitalis, potassium, and mag- 
nesium levels. An antidote (sheep-derived digoxin 
antibody Fab fragments) is effective against some 
plant cardiac glycosides and should be considered 
in life-threatening complications, such as hyperka- 



lemia, high-degree heart block, cardiac arrest, and 
ventricular dysrhythmias. 

See also foxglove; glycoside; lily of the valley; 

OLEANDER. 



carneum A variety of chrysanthemum used in the 
production of the botanic insecticide pyrethrum. 
See also botanic insecticides; pyrethrum. 



Carolina horse nettle (Solanum carolinense) [Other 
names: ball or bull nettle, ball nightshade, sand- 
briar, tread softly.] This member of the Solanum 
family grows from Nebraska to Texas, east to the 
Atlantic and in extreme northern Ohio, southern 
Ontario, and southern Cahfornia. It is a member 
of a very large genus with 1,700 species, most of 
which have not been evaluated toxicologically. 

Poisonous part 

Human poisoning is usually attributed to imma- 
ture fruit, which contains the toxin solanine 
glycoalkaloid. 

Symptoms 

While there is little danger of fatal poisoning in 
adults, children may ingest a fatal amount of this 
plant. Symptoms appear several hours after inges- 
tion and include gastric irritation, scratchy throat, 
fever, and diarrhea (solanine poisoning is often 
confused with bacterial gastroenteritis). 

Treatment 

The same general supportive care that would be 
given in gastroenteritis cases; fluid replacement 
may be required. 

cascabel See rattlesnake, cascabel. 

cassava (Manihot esculenta) [Other names: bitter 
cassava, juca, manioc, manioc tapioca, sweet potato 
plant, yuca.] Found in the tropics, this is a tuber- 
ous edible plant of the spurge family and is culti- 
vated for its roots, from which cassava flour, breads, 
tapioca, laundry starch, and alcoholic beverages are 



54 castor bean 



made. It is believed that cassava was once cultivated 
by the Maya in the Yucatan. Tapioca is the only cas- 
sava product on sale in northern markets. 

If improperly prepared and cooked, cassava can 
cause poisoning to those who eat it, although there 
is no danger if it is prepared properly. Cassava meal 
and tapioca are made from the tuberous plant, but 
the plant must be heated and the poison dissolved 
out before the plant is edible. The two kinds of 
cassava (bitter and sweet) are often confused, but 
the bitter variety is more poisonous. Both require 
careful preparation. 

Cassava appears in many varieties, with usually 
large fan-shaped leaves very much like the castor 
bean. The varieties range from low herbs to tall, 
slender trees and are found in dry areas as well as 
along riverbanks in Guam, Hawaii, the West Indies, 
Florida, and the Gulf Coast states. 

Poisonous part 

Cyanogenetic glycosides (linamarin and lotaus- 
tralin) are broken down in the body to produce 
hydrocyanic acid; they occur in different amounts 
in most varieties. The roots are the most poisonous, 
although the leaves also contain variable amounts. 
Primitive people were able to remove the poison 
by grating, pressing, and heating the tubers. The 
poison amygdalin in the juice breaks down into 
hydrocyanic acid, which can cause cyanide poison- 
ing and has been used for darts and arrows. 

Symptoms 

Experts differ as to how rapidly death can occur, 
with times ranging from within minutes to hours. 
Symptoms can include nausea, respiratory problems, 
twitching, staggering, convulsions, coma, and death. 

Treatment 

Gastric lavage followed by a 2 5 percent solution of 
sodium thiosulfate. 

castor bean (Ricinus communis) [Other names: 
African coffee tree, castor oil plant, gourd, koii, 
man's motherwort, Mexico weed, palma Christi 
(from the shape of its leaves, resembling Christ's 
hand), steadfast, wonder tree.] This is considered 
by some sources to be the most dangerous plant in 



the United States. It is the source of castor oil and 
is also used as a mosquito repellent and a cathartic. 
Castor bean is grown for commercial and orna- 
mental use in the United States and the tropics and 
has become naturalized in Florida, along the Gulf 
and Atlantic coasts, in southern California, and in 
Hawaii. 

A member of the spurge family, castor bean is 
a large annual that grows up to 15 feet high and 
has hollow stems that bear blue-green leaves up to 
three feet across. It produces bronze-red clusters of 
flowers in June followed by spiny seed pods con- 
taining plump seeds; the pods are often removed 
because of the highly toxic content concentrated 
in their seeds. 

Early Americans made a laxative from the 
beans. Native to Africa, the plant is now natural- 
ized throughout the tropics. R. communis is the 
only species in its genus, but there are hundreds 
of varieties. 

Poisonous part 

All parts of the plant (especially the seeds) contain 
the poison ricin, a plant lectin (toxalbumin) that is 
one of the world's most toxic substances. While the 
toxic mechanism of ricin is not well understood, it 
is thought that it inhibits the synthesis of protein 
in the intestinal wall. Small amounts of castor oil 
are also present in the seeds. If the beans are swal- 
lowed whole, the hard seed coat prevents absorp- 
tion and therefore inhibits poisoning, but two to six 
beans can be fatal if well chewed. In a child, one or 
two seeds can be fatal. 

Symptoms 

Usually developing after several hours, symptoms 
include a burning sensation in the mouth, throat, 
and stomach, nausea, vomiting, severe bloody 
diarrhea, abdominal cramps, dulled vision, convul- 
sions, trouble in breathing, paralysis, and death 
from within hours up to 12 days. One to six well- 
chewed seeds may be fatal to a child. Castor beans 
can also induce labor. 

Treatment 

There is no known antidote for ricin poisoning, so 
treatment is primarily supportive and symptomatic. 
Perform gastric lavage immediately, with bismuth 



centipedes 55 



subcarbonate or magnesium trisilicate to line the 
stomach. Fluids and electrolytes must be moni- 
tored. Administration of activated charcoal can be 
successful, since charcoal binds ricin well. 



Catapres (clonidine) One of a group of antihy- 
pertensive drugs designed to lower blood pressure, 
Catapres is considered to be supertoxic in either its 
tablet or injectable form. Once it is administered 
to control blood pressure, an abrupt withdrawal 
of the drug can precipitate a dangerous spike in 
blood pressure, psychosis, hyperexcitability, irregu- 
lar heartbeats, and death. 

Symptoms 

Within 30 minutes after ingestion, an overdose 
causes slow heartbeat, drowsiness, stomach upset, 
rash, low blood pressure, depressed breathing, 
coma, and heart failure. 

Treatment 

Atropine is administered, while monitoring the 
cardiorespiratory system and kidney function. 
See also antihypertensive drugs. 



catfish (Siluriformes) Related to carp and min- 
nows, the catfish gets its name from the four to 
five long whiskers on the upper jaw; many also 
have spines in front of the dorsal and pectoral fins 
that may cause painful stings, especially by young 
catfish. There are about 2,500 species of catfish 
in about 30 families mostly living in fresh water, 
although a few live in the sea. Those who make 
their homes in fresh water are found throughout 
the world and are generally bottom swimmers, 
scavenging on animal or vegetable matter during 
the night. Catfish stings are common and can be 
very painful; they are usually the result of han- 
dling the fish while removing it from hook or net. 
While most varieties cause only a painful sting, the 
venom of one species, Plotosus lineatus (found in the 
Indo-Pacific), can be lethal. 

Symptoms 

While death is rare, the sting of the catfish causes 
an immediate severe stinging or throbbing pain. 



which may stay at the site of the wound or spread 
throughout the body and last for several hours 
or days. There may be redness and swelling at 
the site of the sting, and the area may become 
numb. 

Treatment 

Flush the wound with fresh or salt water, and 
then soak the affected area in hot water or put hot 
compresses on it. The water should be very hot 
(122°F), so that the heat will deactivate the poison. 
Continue applying hot water for 30 minutes to an 
hour. These common stings often become infected, 
and removal of the barb is essential. X-rays can 
determine whether the barb has actually been 
removed; if not, the wound should be opened and 
the spine taken out. Both antibiotics and tetanus 
prophylaxis are indicated. 

centipedes While small centipedes from temper- 
ate zones are harmless, the larger varieties found 
in the tropics can cause pain by injecting venom 
through their claws. The biggest is the giant cen- 
tipede (Scolopendra gigas), which ranges from the 
Southern United States to the West Indies. Cen- 
tipedes are found in loose soil and leaf litter and 
under stones and may not have 100 feet — despite 
their name. 

Poisonous part 

These insects inject toxic substances into the skin 
from a pair of hollow jaws that act hke fangs. The 
venom is relatively weak. The giant centipede is 
the only one in the United States dangerous to 
humans. 

Symptoms 

Generally a mild inflammation at the wound site 
with mild swelling of the lymph nodes. The bite 
of the giant centipede causes inflammation, swell- 
ing and redness and systemic symptoms that fade 
within five hours. 

Treatment 

Apply cool compresses at wound site; for the bite 
of the giant centipede, use cool saline compresses 
with painkillers or sedatives as required. 



56 charcoal, activated 



charcoal, activated This substance, which absorbs 
a wide variety of toxins and renders them ineffec- 
tive, is an indispensable part of any first aid kit. 
Activated charcoal is made from coal, lignite, or 
waste from paper manufacturers, and soft organic 
material like vegetables. It is used to prevent the 
absorption of toxins in the gastrointestinal tract 
within a few minutes of administration. 

Activated charcoal can be effective with most 
chemicals and is considered one of the best, cheap- 
est, and most practical emergency antidotes. For 
maximum effectiveness, activated charcoal should 
be administered within the first hour of poison 
ingestion. The sooner it is given, the more poison 
it is capable of absorbing. 

According to some reports, the recommended 
dosage of activated charcoal is 30-50 grams in four 
ounces of water for children and 50-100 grams in 
8 ounces of water for adults — a dose far larger than 
those included in most home poison kits. 

Activated charcoal will inactivate syrup of ipecac 
and should not be given at the same time. It should be 
administered only after vomiting has been success- 
fully induced. It is nontoxic and is inert if aspirated, 
and there are contraindications to its use. It is not 
used when a neutrahzing agent is administered 
by mouth (such as to treat iodine ingestion or 
mercury, iron, strychnine, nicotine, or quinine 
poisoning). 

In addition, it is not used when a patient is vom- 
iting blood, nor is it effective with certain heavy 
metals such as iron salts or lithium. Activated char- 
coal is also poorly effective with products involving 
alcohol and petroleum distillates and is contra- 
indicated after ingestion of strong acids or strong 
alkalies. It should not be given if analysis of gastric 
contents is necessary, or if the contents need to be 
viewed (to tell the color or number of pills, etc.). 

Caution: 

Giving artificial charcoal too fast usually causes 
vomiting. 

See also ipecac syrup. 



charcoal briquettes A type of compressed fuel 
intended for outdoor use in charcoal grills and 
hibachis. However, in enclosed areas with little 



ventilation, the burning charcoal releases fatal 
amounts of carbon monoxide gas. At least 40 fatali- 
ties have been reported in recent years because of 
the indoor use of such charcoal in campers, trailers, 
tents, boats, apartments, and other enclosed areas. 
See also carbon monoxide. 



chelating agent Chemicals used to treat poison- 
ing by metals such as arsenic, mercury, lead or iron, 
these agents combine with the metal to form a less 
poisonous substance, which is then more quickly 
excreted in the urine. Penicillamine is a common 
chelating agent as is EDTA (ethylene diamine 
tetraacetic acid), which is FDA-approved for treat- 
ment of lead poisoning. 

The word chelate is derived from the Greek chele, 
which refers to the claw of a lobster; this describes 
the pincerlike binding ability of metal ions. 

See also arsenic; lead poisoning; mercury. 

cherries, wild and cultivated (Prunus) Although 
the cherry tree is widely cultivated for its fruit, the 
pits and leaves of the tree are poisonous. 

Poisonous part 

The pits contain cyanogenic glycosides (amygda- 
lin), a substance that, when eaten, releases hydro- 
cyanic acid. 

Symptoms 

Some hours may pass before symptoms appear, 
since the glycosides are not released until they 
are hydrolyzed in the gastrointestinal tract. When 
they do appear, symptoms include shortness of 
breath, vocal cord paralysis, abdominal pain, mus- 
cle twitches, vomiting, lethargy, sweating, and 
weakness. In severe poisoning, symptoms progress 
to seizures, unconsciousness, stupor, and coma. 

Treatment 

Gastric lavage (if conscious) followed by a 25 per- 
cent solution of thiosulfate. If the victim is uncon- 
scious, acidosis is corrected and shock treated, 
together with the administration of oxygen and a 
cyanide antidote. 

See also cyanogenic glycosides. 



children and poisons 57 



cherry pit See Prunus. 

children and poisons Every year in the United 
States, about 10 million cases of poisoning occur. 
Eighty percent of these cases involve a child under 
the age of five years. Poisoning among children 
typically occurs because of curiosity, an inability 
to read warning labels, a desire to imitate adults, 
and inadequate supervision by adults. Despite 
the staggering high number of poisonings in chil- 
dren, only about 50 children die each year from 
a toxic substance, a number that is tragic yet 
remarkable. 

Medications for children 

Children can be poisoned if they have access to a 
medicine cabinet or other place where medications 
have been stored, but it is also possible for them 
to be poisoned if they are given the wrong type or 
amount of medicine. Follow these safe-medicine 
guidehnes at all times: 

• Follow medicine label directions carefully to 
avoid accidental overdoses. 

• If anything about label directions on your child's 
prescription medicines seems different, unusual 
or odd, CALL THE PHARMACIST IMMEDIATELY. 
Do not assume that a mistake is impossible. 

• Never give your child medicine in the dark. 
Many medicine bottles look ahke in dim light. 
Take the time to be sure you are dispensing the 
correct medication. 

• Know your child's current accurate weight; 
weight affects dosage. 

• Do not substitute a kitchen teaspoon for a mea- 
suring teaspoon when giving medicine. 

• Properly dispose of unused and outdated 
medications. 

• Do not use prescription medication for anyone 
other than the person it was prescribed for. 

• Never refer to medicine as "candy" to a child. 

• Avoid taking your medicine in front of your child, 
since youngsters like to imitate grown-ups. 

• When you are using medicine or giving it to 
someone else, never let young children out of 



your sight, even if that means taking them along 
to answer the phone or the door. 

Just because you can buy medicine without 
a prescription does not mean that the medicine 
is safe if taken in overdose. The painkiller acet- 
aminophen is one of the most commonly misused 
medications during childhood. Because it's been 
available over the counter for years and is sold in 
a variety of dosage formulations, most parents feel 
very comfortable in giving acetaminophen for pain 
or fever. However, studies have found that many 
parents give too much of the drug too often. In fact, 
it is not uncommon for parents to give their chil- 
dren adult dosages, which can lead to significant 
liver disease and even death. 

While acetaminophen is the nonprescription 
drug most often given in error, parents also make 
mistakes with other over-the-counter products, 
including cold medications, antihistamines, and 
cough suppressants. 

Medicine cabinet safety 

The key to keeping the home safe from poisons is 
to go room by room and poison-proof the whole 
place. The best starting point is probably the 
bathroom medicine cabinet, where most people 
store all the family's medications. (Actually, the 
bathroom is the worst place to store medicine; 
the moist, warm environment tends to change or 
degrade the chemicals.) Follow these guidelines to 
make sure your medicines are stored safely: 

• Keep pills in their original containers. 

• Always close and put away the container as soon 
as you are finished using it. 

• Always keep medicines out of sight and out of 
reach of children. 

• To prevent toddlers or kids from getting into 
cabinets, consider buying a "cabinet lock" for the 
medicine chest. 

• Always use child-resistant caps. 

• Remember that child resistant does not mean 
childproof. To be legally designated as "child resis- 
tant," the container must take more than five min- 
utes for 80 percent of five-year olds to open (which 
means that 20 percent can get into it in less time). 



58 children and poisons 



• Never keep medicine on a countertop or bedside 
table. 

• Clean out the medicine cabinet from time to 
time, and throw out all unneeded medicine once 
the illness it treated is over. Pour contents down 
the drain or the toilet and rinse out the container 
before throwing away. 

• Never assume that children will not take or 
could not have taken a medication because it 
tastes bad to you. 

• Never assume that children will not take or 
could not have taken a medication because it is 
too big for them to swallow. 

•Be especially careful about medicine in handbags 
and suitcases, which may be left unprotected 
around the house. 

Toxins, in infants and toddlers 

The most important thing to remember is this: 
babies are not tiny adults. Because babies have a low 
body weight, a very small amount of a potentially 
harmful substance can have a toxic effect. Another 
factor is that infants and young children grow 
rapidly, and so any chemicals to which they are 
exposed can be incorporated into their body tis- 
sues in high amounts. Compounding this problem 
is that infants and toddlers have immature intes- 
tines, liver, and kidneys — the organs responsible 
for detoxifying substances — as well as a nervous 
system (including the brain) that is extremely vul- 
nerable to environmental toxins. 

Although parents need to be extremely care- 
ful about exposing their children to toxic sub- 
stances, some items are considered to be nontoxic 
to children unless they are ingested in very large 
amounts. That is not to say that these substances 
will not cause some symptoms; however, they are 
generally nontoxic to children. These nontoxic 
substances are listed in the accompanying table. 

Nontoxic Substances 

antacids 
antibiotics 
aquarium products 
baby oil 

birth control pills 
blackboard chalk 



bubble bath 
candles 

caps for a cap pistol 
castor oil 
cosmetics 

dehumidifying packets 

denture adhesive 

deodorants 

diaper rash ointment 

dry cell batteries 

eye makeup 

fabric softener 

glycerin 

graphite (in "lead" pencils) 

hand creams and lotions 

kaolin 

lanolin 

lauric acid 

lipstick 

modeling clay 

multivitamins (without iron or fluoride) 
nail pohsh 
petroleum jelly 
putty 

shaving cream 
soaps 

stearic acid 
tallow 

teething rings 
watercolor paints 

Poison in toys 
Toxic children's toys have become a critical issue 
in recent years, and the Consumer Product Safety 
Commission (CPSC) has recalled millions of toys 
believed to contain dangerous amounts of lead 
paint or other toxic substances. In April 2006, 
it was reported that there was lead in children's 
necklaces that had been shipped from China and 
sold in the United States at Dollar General stores 
from January 2003 through December 2005 for 
one dollar apiece. In June 2007, the CPSC recalled 
1.5 million Thomas and Friends wooden railway 
toys that contained lead paint. In September 2007, 
Mattel recalled 675,000 Barbie Accessory toys 
because of high levels of lead paint. In Novem- 
ber 2007, a toy called Aqua Dots, imported from 
China, consisted of beads that had a chemical coat- 



chloral hydrate 59 



ing on them. When the beads were ingested, the 
chemical metabolized into gamma hydroxybutyr- 
ate, a date rape drug, with the potential to cause 
unconsciousness, seizures, drowsiness, coma, and 
death. No deaths were associated with ingesting 
the beads, but most of the affected children were 
hospitalized. 
See also lead. 



chinaberry (Melia azedarach) [Other names: Afri- 
can lilac tree, bead tree, China tree, false syca- 
more, hog bush, Indian lilac, Japanese bead tree, 
paradise tree, Persian lilac, pride of China, pride of 
India, Texas umbrella tree. West Indian lilac, white 
cedar.] Found in the southern United States 
from Virginia to Florida west to Texas, in Hawaii, 
the West Indies, and Guam, the chinaberry tree 
grows as high as 50 feet, with 2-inch-long ser- 
rated leaves and fragrant purple flower clusters. 
The yellow fruit contains up to five smooth black 
seeds. 

Poisonous part 

Fruit and bark contain tetranortriterpene neu- 
rotoxins and unidentified gastroenteric toxins; 
toxicity varies considerably depending on the con- 
centration of toxin in the plant. 

Symptoms 

Following a fairly long latency period, symptoms 
include faintness, confusion, stupor, vomiting, 
and diarrhea, which can lead to shock. Breath- 
ing problems may be followed by convulsions, 
paralysis, and, very rarely, death. While six to eight 
fruits can be lethal to a child, human exposures in 
the United States are generally limited to severe 
gastroenteritis. 

Treatment 

Replace fluids and electrolytes, give activated char- 
coal, and treat symptoms. Kidney and liver func- 
tion should be monitored. There is no antidote. 



chinchonism A syndrome produced by overdose 
of quinine, sahcylates, and cinchophen, consist- 
ing of ringing in the ears, hearing and balance 



problems, blurred vision, photophobia, headache, 
nausea, vomiting, diarrhea, flushed skin, sweating, 
fever, and skin rash. 

See also cinchophen; quinine; salicylates. 



chloral hydrate The well-known "Mickey Finn" 
or "knockout drops" popularized in the detective 
fiction of the 1930s, chloral hydrate is the oldest 
prescription sleeping pill available today. It was 
introduced in 1862 as a derivative of chloroform 
and quickly became a popular drug of abuse dur- 
ing those years; it is one of five sedative-hypnotic 
drugs introduced before 1900. 

Symptoms 

A central nervous system depressant, chloral 
hydrate in therapeutic doses produces drowsiness 
within 30 minutes after ingestion, followed by a 
sound sleep within an hour. Unlike with other 
sedatives, under normal conditions there is rarely 
a hangover afterward. However, doses larger than 
2 grams can cause poisoning, and the reported 
fatal dose is between 5 and 10 grams. The toxicity 
of chloral hydrate does vary considerably but in 
general acts in three ways: depressing the central 
nervous system, corroding the skin and mucous 
membranes, and affecting some major organs. 
Ingested in large amounts, chloral hydrate causes 
sleepiness, confusion, clumsiness, slow and shallow 
breathing, weakness, low blood pressure, cyanosis, 
and a deep coma within 30 minutes of ingestion. 
It may be fatal in a few hours — or even sooner, as 
a result of respiratory collapse. In addition, there 
may be kidney and liver damage. 

Chloral hydrate can also cause chronic poison- 
ing, resulting in a skin rash, confusion, dizziness, 
drowsiness, depression, and a wide range of behav- 
ioral abnormalities, including irritability, poor judg- 
ment, and a general lack of interest in personal 
appearance. 

Chloral hydrate is radiopaque, and diagnosis 
of overdose can be confirmed with an abdominal 
X-ray. 

Treatment 

There is no known antidote to chloral hydrate 
poisoning. Treatment is similar to poisoning with 



60 chloramine gas 



other narcotics: gastric lavage (only if begun soon 
after ingestion, because of this drug's rapid absorp- 
tion in the gastrointestinal tract). Since onset of 
action is so rapid, induced vomiting could be dan- 
gerous. Afterward, administer activated charcoal 
and provide demulcents (such as milk). Provide 
supportive treatment (including oxygen). Hemodi- 
alysis may also be effective. 

chloramine gas A deadly gas that results from 
the combination of ammonia and cleaners contain- 
ing hypochlorite salts. For this reason, two differ- 
ent types of household cleansers should never be 
mixed. 

Symptoms 

Breathing these fumes can cause headache, eye irri- 
tation, dizziness, visual disturbances, and nausea. 

Treatment 

Remove victim from contaminated air; observe for 
breathing problems. 

Chloramine-T (sodium p-toluenesulfochloramine) 

This drinking water disinfectant and deodorant 
contains 12 percent chlorine, which is slowly 
released on contact with water; as a solution, it 
is used as a mouthwash. It is also used to remove 
odor from cheese. 

Symptoms 

It is believed that this compound works by trans- 
forming chloramine-T into a derivative of cyanide, 
resulting in cyanosis, respiratory failure, collapse, 
and frothing at the mouth. Death follows within a 
few minutes. It is suspected of causing rapid allergic 
reactions in hypersensitive victims. 

Treatment 

Gastric lavage, followed by the administration of 
sodium nitrate and sodium thiosulfate. Patients 
who survive 24 hours are expected to recover. 

chlorate poisoning Chemicals used in some defo- 
liant weed killers and in industries to make dyes. 



explosives, or matches can cause kidney, liver, and 
intestinal damage and can be fatal in small doses, 
especially in children. 

Symptoms 

Ulcers in the mouth, abdominal pain, and 
diarrhea. 

Treatment 

If spilled onto skin or eyes, wash off immediately 
with water. If ingested, seek medical help imme- 
diately. Methylene blue is effective only if given 
in the very early stages. Otherwise, gastric lavage, 
exchange transfusion, bicarbonate infusion, hemo- 
dialysis, and heparin are suggested. 

chlordane (1,2,4,5,6,7,8,8 octachloro-4,7-methano- 
3a,4,7,7a-tetrahydroindane; chlordan octachloro- 
tetrahydro methane indane) [Trade names: CD-68, 
Dowklor, Octa-Klor, Ortho-Klor, 1068, Toxichlor, 
Velsicol 1068.] One of a group of synthetic 
organochlorine pesticides, chlordane is a viscous 
liquid with a chlorine odor ranging from color- 
less to amber. Introduced in 1945, use and com- 
mercial production have been prohibited in the 
United States and many other countries since 1988, 
because it does not disperse in the environment but 
instead accumulates in biological systems. 

It dissolves in both water and fat and is available 
as a powder, dust, emulsion concentrate and a con- 
centrated solution in oil. Skin absorption is rapid, 
but reports of human poisonings are limited. 

Symptoms 

Chlordane is a fairly quick acting chemical and less 
toxic than similar pesticides, but still toxic; violent 
convulsions appear suddenly within 30 minutes 
to three hours after ingestion. The first 12 hours 
are the most dangerous, and death — if it is likely 
to occur — will usually take place within this time 
frame. It is possible, however, that a person will 
live up to 20 days after ingestion before finally suc- 
cumbing. Other symptoms include liver damage 
and congestion in the brain, lung, heart, and spinal 
cord. The estimated lethal oral dose of chlordane 
in an adult is 3-7 grams. It has been implicated in 
acute blood abnormalities. 



chlorine 61 



Treatment 

There is no specific antidote. Perform gastric lavage, 
but do not induce vomiting because of the risk of 
sudden onset of seizures; administer activated 
charcoal and a cathartic. Irregular heartbeat may 
respond to propranolol. If convulsions last for some 
time, recovery is unlikely. 

See also chlorinated hydrocarbon pesticides. 

chlorinated hydrocarbon pesticides This group 
of insect-fighting chemicals was once widely 
used in agriculture and malarial control programs 
around the world from the 1940s through the 
1960s, However, environmental contamination 
has led to their disfavor; DDT and chlordane, for 
example, are banned from commercial use because 
they do not disperse in the environment and 
because they accumulate in biological systems. 
Some have been shown to cause cancer in humans, 
including chloroform, vinyl chloride, aldrin, chlor- 
dane, dieldrin, heptachlor, lindane, toxaphene, and 
carbon tetrachloride. Instead, organophosphates 
(such as malathion and diazinon) have more or less 
replaced the chlorinated hydrocarbons, since they 
control insects, are biodegradable and (according 
to their manufacturers) do not contaminate the 
environment. 

The most highly toxic of the group are aldrin, 
dieldrin, endrin, and endosulfan; moderately toxic 
are chlordane, DDT, heptachlor, kepone, lindane, 
mirex, and toxaphene; slightly toxic are ethylan 
(perthane), hexachlorobenzene, and methoxychlor. 

As a group, these insecticides interfere with 
the transmission of nerve impulses throughout 
the body (especially the brain), causing behavior 
changes, involuntary movements and depressed 
respiratory system. They may also cause liver or 
kidney damage and may also be carcinogenic. In 
general, the route of poisoning is through the skin 
(especially with aldrin, dieldrin, and endrin). 

Symptoms 

Soon after these chemicals are ingested, symp- 
toms of nausea and vomiting appear followed by 
confusion, tremor, coma, seizures, and respiratory 
depression. There have been reports of delayed and 
recurrent seizures and irregular heartbeat. 



Treatment 

There is no specific antidote for chlorinated hydro- 
carbon poisoning. Treat symptoms and perform 
gastric lavage, but do not induce vomiting. Then 
administer activated charcoal and a cathartic. 

See also chlordane; DDT; dieldrin; endrin; lin- 
dane; MIREX. 

chlorine This yellow-green gas with an irritating 
odor is widely used to manufacture chemicals, as 
a swimming pool disinfectant and cleaner, and as a 
bleach. Chlorine and chlorine -containing compounds 
are also found in table salt (sodium chloride), plastics 
(polyvinyl chloride), aerosol propellants (chlorofluo- 
rocarbons), and pesticides, as well as throughout the 
body in all nerve and muscle tissues. 

Chlorine was also used briefly as a chemical 
weapon during World War I, but it was subse- 
quently replaced by other chemicals. Current toxic 
exposures come from accidental spills and the 
improper use of household products. A deriva- 
tive of chlorine's derivative, hypochlorite, is found 
in most household bleaches in solutions of 3 to 
5 percent; adding ammonia to this hypochlorite 
solution may release chloramine, which can cause 
unconsciousness, especially if the area is small and 
unventilated. However, a person would need to 
be in the fumes for more than an hour for serious 
problems to develop. Adding an acid to hypochlo- 
rite solution releases chlorine gas. 

A natural chemical element and a gas at room 
temperature, chlorine is easily liquefied under 
pressure. Pure chlorine rarely occurs in nature, 
except in volcanic eruptions — and even then, the 
quantities released are small. 

Accidental spills or leaks of chlorine gas during 
transport or storage are the greatest exposure haz- 
ard today; in the event of such a spill, whole neigh- 
borhoods or towns may be evacuated. Chlorine and 
hydrochloric acid rank first and third respectively 
in causing injuries and deaths from large accidents 
involving industrial chemicals, although the actual 
number of incidences is small. 

Symptoms 

When in contact with moist tissue (such as the eyes 
and upper respiratory tract), chlorine gas is a strong 



62 chlorine gas 



irritant and causes corrosive injury; aqueous solu- 
tions of chlorine also cause corrosive injury to eyes, 
skin, and gastrointestinal tract. Inhaling chlorine 
gas causes immediate burning of eyes, nose, and 
throat, with coughing and wheezing. More seri- 
ous poisoning results in croupy cough, hoarseness, 
and upper airway swelling to the point of obstruc- 
tion. In quite severe cases of poisoning, pulmonary 
edema may result. Skin or eye contact with either 
the gas or the concentrated solution causes corro- 
sive burns. Ingestion of 3-5 percent hyperchlorite 
solution is not particularly serious, causing an 
immediate burning in the mouth and throat but 
no further injury. More concentrated solutions 
may result in serious esophageal and gastric burns, 
together with drooling and severe throat, chest, 
and abdominal pain and with perforation of the 
esophagus or stomach. 

There is a slight increase in the risk of bladder 
cancer and possibly colon and rectal cancers in 
longtime users of chlorinated water supplies. 

Hypochlorite in bleach is a corrosive substance 
that can damage skin, eyes and other membranes. 
According to poison control centers, a high number 
of children each year accidentally swallow laun- 
dry bleach, although relatively few fatalities are 
reported (probably because of the vomiting that 
bleach causes). However, damage to the esophagus 
and stomach can occur. 

Treatment 

While many experts recommend administration 
of corticosteroids in an attempt to limit esopha- 
geal scarring, this treatment is unproven and may 
be harmful in those with perforations or serious 
infection. For the inhalation of chlorine gas, give 
humidified supplemental oxygen, and observe for 
signs of upper airway obstruction. Treat symptoms. 
For ingestion of hyperchlorite solution greater than 
10 percent (or with symptoms of corrosive injury), 
check for serious esophageal or gastric injury with 
a flexible endoscope. A chest X-ray will also reveal 
a perforated esophagus. 

For contaminated skin and eyes, flush exposed 
skin with water; irrigate eyes with water or saline. 
For ingestion of hypochlorite solution, immedi- 
ately give water or milk by mouth. Do not induce 
vomiting; perform gastric lavage after concentrated 



liquid ingestion. Do not use activated charcoal, 
since it may interfere with the endoscopist's view. 
See also chlorine gas. 



chlorine gas This yellow-green gas is used in the 
manufacture of plastics, purified water, cloth, and 
paper and usually causes poisoning after a leak in 
a storage tank. The damage following exposure to 
chlorine gas depends on its concentration, duration 
of exposure and the water content of the exposed 
tissue, but it is capable of causing rapid and exten- 
sive tissue destruction. Chlorine gas is 30 times 
more toxic to cells than hydrochloric acid. 

Symptoms 

Skin contact causes severe burns; inhalation of 
gas at greater than three to six parts per million 
causes conjunctivitis, keratitis, sore throat, burning 
chest pain, and coughing. A moderate exposure 
causes immediate, severe irritation of the mucous 
membranes of the nose, throat, and eyes, with a 
distressing cough. Excessive exposure results in a 
severe, productive cough, difficulty in breathing, 
and cyanosis. There may be prolonged vomiting, 
restlessness and anxiety, followed by lack of oxy- 
gen and heart attack. 

Treatment 

Remove the victim from the environment. Wash 
eyes with saline after the apphcation of topical 
anesthesia. Burns should be washed with saline; 
hospitalization may be necessary. Bronchodilators 
and humidified oxygen will alleviate breathing 
problems, together with the administration of 
steroids. 

See also chlorine. 



chlorobenzene derivatives These chemicals are 
a type of synthetic organic insecticide and include 
DDT, TDE, DFDT, DMC, neotrane, ovotran, and 
dilan. They are soluble in fat (not water), and 
according to reports, the amount of these chemicals 
present in the body fat of individuals in the United 
States is higher than in Canada, England, France, 
and the former West Germany. In those prepara- 
tions that are still legally available, the commercial 



Christmas rose 63 



solutions are sold in dry mixtures or in solutions 
of one or more inorganic solvents (kerosene, ben- 
zene, etc.), which are also toxic in themselves. 

Symptoms 

These compounds affect the central nervous system 
and result in restlessness, irritability, muscle spasm, 
tremor, and convulsions followed by depression, 
collapse, and breathing problems due to respira- 
tory failure. Absorption through the skin or by 
inhalation causes eye, nose, and throat irritation, 
blurred vision, pulmonary edema, and skin prob- 
lems. Chronic poisoning symptoms include loss of 
weight, liver, and kidney damage, and disturbances 
of the central nervous system. 

Treatment 

Gastric lavage followed by saline cathartics. Avoid 
all fats and oils (including milk), since they increase 
the rate of absorption of chlorinated hydrocarbons. 
Administer phenobarbital sodium for tremors, and 
barbiturates for convulsions, and provide oxygen 
if necessary. If the skin has come in contact with 
these insecticides, wash with soap and water 
immediately to head off skin problems and sys- 
temic absorption. Remove contaminated clothing. 
See also DDT; insecticides. 

chloroform (trichloromethane) This chlorinated 
hydrocarbon solvent is used in the production of 
Freon and as a solvent in the chemical and phar- 
maceutical industries; it is a direct central nervous 
system depressant. 

It was discovered independently and simultane- 
ously in 183 1 in Germany, France, and the United 
States, and accounts of its abuse were reported in 
the United States in that same year. Dentist Horace 
Wills, the first person in the United States to use 
nitrous oxide in surgery, died from comphcations 
resulting from his own chronic chloroform abuse. 
Chloroform was introduced as an anesthetic during 
surgery in 1847; it became so popular that Queen 
Victoria knighted its discoverer. Dr. James Simp- 
son, after he delivered her eighth child. 

However, as other anesthetics were discovered 
and the number of overdoses of chloroform rose, its 
medical use lost favor. It has since been abandoned 



because of the toxic effects on the liver, which can 
progress to fatal cirrhosis. In addition, about 10 
percent of the population have a genetic response 
to chloroform that results in an uncontrolled high 
fever (above 110°F) during or after anesthesia. 

Chronic low levels of the chemical may still be 
found in some municipal water supplies. 

Symptoms 

In addition to its effects on the central nervous 
system, chloroform may also cause heartbeat irreg- 
ularities and damage the liver and kidneys. Chlo- 
roform is also toxic to the fetus and is a suspected 
carcinogen. Ingestion or inhalation causes a mild 
to moderate systemic toxicity, including headache, 
nausea, vomiting, confusion, and drunkenness fol- 
lowed by coma, respiratory arrest, and heartbeat 
irregularities. Kidney and liver failure may be dis- 
covered up to three days after exposure. 

Treatment 

If skin or eyes have come in contact with chloro- 
form, remove affected clothing and wash with soap 
and water; irrigate eyes with tepid water or saline. 
If inhaled, remove the victim from the area and 
give oxygen. If ingested, perform gastric lavage, 
but do not induce vomiting (chloroform is rapidly 
absorbed and may depress the central nervous sys- 
tem). Administer activated charcoal and a cathar- 
tic; provide supportive treatment. Acetylcysteine 
may help prevent kidney and liver damage. 
See also anesthetics, gaseous /volatile. 

chlorthion See organophosphate insecticides. 



choke cherry pit See Prunus. 

Christmas rose (Helleborus niger) Also called 
black hellebore or winter rose, this very poisonous 
plant of the buttercup family is found in the north- 
ern United States and Canada and blooms from 
late fall through early spring — often in the snow. 
Its groups of evergreen leaflets resemble fingers on 
a hand; its flowers are white to pinky green and 
appear during Christmas in milder climates. The 



64 chromium 



Christmas rose is found in damp, shady places and 
is closely related to the later-blooming Lenten rose 
(H. orientalis). 

Poisonous part 

All parts of the plant contain the digitalis-like 
glycosides helleborin, hellebrin; and the direct irri- 
tants saponins and protoanemonin. 

Symptoms 

Within 30 minutes after ingestion, the poison will 
blister the mucous membranes in the mouth, with 
abdominal pain, severe diarrhea, vomiting, and 
death from cardiac arrest. The amount ingested 
will determine the length of time between inges- 
tion and the appearance of symptoms; generally, 
poisoning symptoms include conduction defects 
and sinus bradycardia. 

Treatment 

Amyl nitrate, strychnine, and atropine are often 
used as cardiac and respiratory stimulants. Perform 
gastric lavage or induce emesis, and activated char- 
coal may be given repeatedly. 

See also buttercup; glycoside; saponin. 

chromium This silver metal is used by electro- 
platers, welders, lithographers, and metal or textile 
workers and can be toxic by skin contact, inhala- 
tion, or ingestion. 

Poisonous part 

Trivalent chromium compounds (chromic oxide, 
chromic sulfate) and chromate salts of lead, zinc, 
barium, bismuth, and silver do not readily dissolve 
in water and, because they are poorly absorbed, are 
not very toxic. Hexavalent compounds (chromium 
trioxide, chromic anhydride, chromic acid, and 
di chromate salts) do dissolve in water and are more 
easily absorbed by the lungs, gastrointestinal tract, 
and skin. Some of the hexavalent compounds are 
also carcinogenic. 

Symptoms 

Skin/eyes: contact with the skin may cause severe 
burns; contact with the eyes can cause serious 
corneal injury. There have been reports of fatalities 



after skin contact causing only 10 percent burned 
surface area, because the skin burns enhance 
absorption. Inhalation: symptoms (which may 
appear several hours after exposure) include upper 
respiratory tract irritation, wheezing, and pulmo- 
nary edema. Ingestion: there may be immediate 
gastroenteritis, with massive fluid and blood loss 
leading to shock and kidney failure. Other symp- 
toms include hepatitis and cerebral edema. Serious 
poisoning has occurred from ingesting as little as 
500 mg of hexavalent chromium. 

Treatment 

Treat symptoms; chelation therapy is not effec- 
tive. Skin/eyes: wash exposed area with soap and 
water (for eyes, flush with tepid water or saline). 
Inhalation: give supplemental oxygen if necessary. 
Ingestion: (of hexavalent compounds) ascorbic acid 
may be administered; give milk or water to dilute 
corrosive effects, and perform gastric lavage, but do 
not induce vomiting because of the potential for 
corrosive injury. Administer activated charcoal. 

ciguatera Ciguatera poisoning occurs after eat- 
ing any of more than 300 species of fish that may 
contain a type of toxin undetectable by inspection, 
taste, or smell. The fish are toxic at certain times of 
the year when they ingest a specific type of plank- 
ton that contains "ciguatoxin." Ciguatoxin is an 
odorless, tasteless poison that can not be destroyed 
by either heating or freezing. 

Ciguatoxin is usually found in larger coral-reef 
fish, including barracuda, snapper, amberjack, sur- 
geon fish, sea bass, and grouper. Other species of 
warm-water fish, such as mackerel or triggerfish, 
may also be contaminated. Not all fish of a given 
species or from a given locality will be toxic at the 
same time. 

Ciguatera occurs most often in the Caribbean 
islands, Florida and Hawaii, and the Pacific Islands. 
Recent reports recorded 129 cases over a two-year 
period in Dade County, Florida, alone. It appears to 
be occurring more often, probably because of the 
increased demand for seafood around the world 
and its recurrence in edible fish. Experts believe 
this type of poisoning is underreported because it is 
usually not fatal and symptoms don't last long. 



clematis 65 



Isolated instances of ciguatera poisoning fiave 
occurred along the eastern United States coast, 
from south Florida up to Vermont. Hawaii, the U.S. 
Virgin Islands, and Puerto Rico also report sporadic 
cases. 

Poisonous part 

The toxin involved in this type of poisoning is 
ciguatoxin, which is found in greatest concentra- 
tion in internal organs. 

Symptoms 

There are both stomach and neurologic symp- 
toms, with a curious type of sensory reversal, 
so that picking up a cold glass would cause a 
burning hot sensation. Other symptoms include 
a tingling sensation in the lips and mouth fol- 
lowed by numbness, nausea, vomiting, abdominal 
cramps, weakness, headache, vertigo, paralysis, 
convulsions, and skin rash. Coma and death from 
respiratory paralysis occur in about 12 percent of 
cases. Subsequent episodes of ciguatera may be 
more severe. Ciguatera is usually self-limiting and 
subsides within several days. 

Complications 

Sometimes, the neurological symptoms may persist 
for weeks or months. Occasionally, symptoms have 
lasted for several years, or patients have relapsed. 
These relapses may be associated with alcohol or 
dietary changes. Rarely, death occurs from breath- 
ing or heart failure. 

Treatment 

Some experts suggest pralidoxime chloride is an 
effective antidote. Other treatment is supportive. 

Prevention 

The only way to prevent this infection is to avoid 
tropical reef fish, since there is no easy way to rou- 
tinely measure the toxin in any seafood product 
before eating. 

See also dinoflagellate; shellfish poisoning. 



cimetidine (Tagamet) An ulcer-healing drug 
related to antihistamines, cimetidine was first 
introduced in 1976. It reduces the secretion of 



hydrochloric acid in the stomach and helps heal 
gastric and duodenal ulcers and heals inflamma- 
tion of the esophagus. 

Symptoms 

On rare occasions, an overdose (or even a thera- 
peutic dose) produces a toxic psychosis within a 
few hours of ingestion, with confusion, disorienta- 
tion, agitation, and hallucinations. Symptoms will 
usually clear within 24 hours. 

Treatment 

Treat symptoms of agitation with gastric lavage; 
barbiturates may be used cautiously to control cen- 
tral nervous system stimulation. 
See also antihistamines. 



cinchophen A painkiller used to treat gout, it is 
available in both oral and injectable form. Cincho- 
phen carries the risk of liver damage, which makes 
its use in the treatment of gout dangerous. 

Symptoms 

Appearing between six and 12 hours after inges- 
tion, symptoms include gastrointestinal irritation, 
anorexia, diarrhea, vomiting, high fever, delirium, 
convulsions, coma, and death. 

Treatment 

Treatment is the same as with salicylate poisoning 
(induce vomiting or perform gastric lavage fol- 
lowed by activated charcoal and a cathartic). 

clematis Many different species of this popu- 
lar and quite beautiful flowering climber can be 
found throughout Canada and the north temperate 
United States. 

Poisonous part 

The whole plant is poisonous and contains the 
toxin protoanemonin, which irritates both the skin 
and the mucous membranes. 

Symptoms 

Ingestion causes intense pain, blistering, and 
inflammation in the mouth and throat together 



66 climbing lily 



with excess salivation, bloody diarrhea, abdominal 
cramps, dizziness, and, in severe cases, convulsions 
and mental confusion. 

Treatment 

Usually, the immediate pain upon chewing leaves 
or flowers limits the amount of toxin ingested. In 
cases of large amounts of poisoning, gastric lavage 
should be performed and demulcents administered. 
Kidney function should be monitored. 

climbing lily (Gloriosa rothschildiana; G. superba) 

Also called glory lilies, climbing lilies have striking 
bright crimson and yellow flowers with finger-like 
petals and lance-shaped leaves tipped with ten- 
drils. They are primarily cultivated in the southern 
United States, the West Indies, and Hawaii. 

Poisonous part 

The entire plant contains the toxin colchicine, 
especially the fleshy, tuberous roots. 

Symptoms 

Immediately after ingestion, the victim experiences 
burning pain in the mouth and throat with intense 
thirst followed by nausea and vomiting. Within 
two hours, abdominal pain and severe diarrhea 
develop, which may lead to shock. There is some- 
times kidney damage. Because colchicine is not 
readily excreted, illness can last for some time. 

Treatment 

Give fluids, and monitor blood pressure and kidney 
function. Administer atropine and painkillers. 

Clostridium botulinum The deadliest known 
type of food poisoning is botulism, which is caused 
by the Clostridium hotulinum toxin, the most poison- 
ous substance in the world. In fact, the fearsome 
reputation of botulism is well deserved, since two- 
thirds of botulism victims die. Those who survive 
face a long recovery period. The bacteria's resis- 
tance to heat makes the spores an important cause 
of poisoning in improperly cooked or canned foods. 
While still fairly uncommon, botulism occurs more 
often in the United States than anywhere else in 



the world due to the popularity of home-canning; 
there are about 20 cases of foodborne botulism 
poisoning in the United States annually. 
See also botulism. 



Clostridium perfringens This type of bacteria, a 
close cousin of C. botulinum, can produce a dan- 
gerous toxin that multiplies quickly in reheated 
foods, which is why it's known as the "cafeteria 
germ." It's often found in foods served in large 
amounts, such as in school cafeterias and hospi- 
tals, left in inadequately heated steam tables or at 
room temperature. It exists in undercooked beef, 
meat pies, stews, burritos, tacos, enchiladas, and 
reheated meats or gravies made from beef, turkey, 
or chicken. Once eaten, the bacteria produce a 
toxin in the digestive tract about six hours later; 
however, a large amount of the bacteria must be 
eaten in order to cause illness. 

This type of food poisoning is very common in 
the United States, with an estimated 10,000 cases 
occurring each year, according to the U.S. Centers 
for Disease Control and Prevention. Outbreaks 
have been often traced to restaurants, caterers, and 
cafeterias that don't have adequate refrigeration 
facilities. Most cases go unreported. 

Symptoms 

Symptoms appear suddenly (within eight to 24 
hours after eating) and include severe cramps and 
abdominal gas pains followed by a 24-hour bout of 
watery diarrhea. There may be nausea but usually 
no vomiting or fever. While usually a mild illness, 
it can be dangerous to infants and the elderly, who 
may become dehydrated. A person can get this ill- 
ness more than once, but a patient is not infectious. 

Diagnosis 

A test can detect the presence of the bacterium. 
The bacteria will also grow on a culture plate in a 
lab from either the food or a stool sample. 

Treatment 

Drink small sips of clear fluids or electrolytes to 
replace what is lost. If you are dehydrated, seek 
medical help. 



cobra, Egyptian 67 



Prevention 

The bacteria produce spores, a dormant form of 
bacteria that isn't killed by cooking. However, the 
spores can't reproduce into bacteria at tempera- 
tures below 40°F or above 140°F. Therefore, keep 
hot foods hot and cold foods cold and don't keep 
reheating and reusing leftovers for several meals. 

clove cigarettes See phenol. 

cobra A large group of highly poisonous snakes 
of the family Elapidae, most of which expand the 
neck ribs to form a hood. Most species of cobras are 
found in warm regions of Africa and are favorites 
of snake charmers. Cobra bites are fatal between 10 
and 50 percent of the time, depending on the spe- 
cies; if untreated, they can be fatal within minutes 
to several hours. 

Cobras that are found in the East have fang 
openings facing forward, enabling the snake to spit. 
Snakes that spit their venom usually direct the poi- 
son at the victim's eyes at distances of up to more 
than 7 feet; the venom can cause temporary or per- 
manent blindness unless promptly washed out. 

These snakes live in holes in the ground, and 
while they can climb into a shrub looking for food, 
they are usually seen underfoot. They are consid- 
ered fairly placid, preferring to flee rather than 
fight. An angry cobra surprised in its hole will hiss 
loudly; if disturbed in the open, it will turn and 
face its victim, inflating its hood and looking very 
fierce. However, its striking range is limited, and it 
will often strike with its mouth closed in the hope 
of discouraging an attacker. 

Included in the cobra family are the Indian or 
Asian cobra, the Egyptian or African cobra, the 
ringhals, the black-necked cobra, and the tree cobra. 
Those of the cobra family without hoods include 
the blue krait, pama, black mamba, green mamba, 
taipan, death adder, tiger snake, Australian black 
snake, brown snake, eastern coral, Arizona coral, 
African coral, black-banded coral, and the Brazilian 
giant coral. 

Symptoms 

The venom of a cobra snake is a toxin chemically 
different from that of other snakes; some suggest it 



may contain a cardiotoxin. Within 1 5 to 30 minutes 
symptoms appear: pain, swelling, a drop in blood 
pressure, confusion, slurring of speech, dilation of 
the pupils, strabismus (deviation of the eye), droop- 
ing of the upper eyehd, and muscle weakness. The 
respiratory muscles are affected last, and respira- 
tory muscle paralysis is the most common cause of 
death. The venom from this snake family is twice as 
toxic as strychnine and nearly five times more toxic 
than the venom of a black widow spider. 

Treatment 

The specific antiserum for the type of cobra involved 
should be used. 

cobra, black-necked See cobra, spitting. 

cobra, Egyptian (Naja haje) Most likely the asp 
of ancient history and of Cleopatra's suicide, the 
Egyptian cobra is dark with a narrow hood. It 
inhabits much of Africa, in the savanna and some- 
times near water, and has also been seen in a few 
small areas in Saudi Arabia. Also known as the 
African cobra, it is quiet but inquisitive and highly 
aggressive when restrained. It is considered small 
but can grow as long as 6 feet. 

Cobras live in holes in the ground, and while 
they can climb into a shrub if they have to, it is 
unusual to see them anywhere but on the ground. 
These snakes will hiss if threatened in their holes, 
but if threatened in the open, they will pack their 
coils around themselves, spread their hoods and 
turn to face the enemy. 

Symptoms 

Within 15 to 30 minutes symptoms appear: pain, 
swelling, a drop in blood pressure, and confusion 
followed by death if the poison spreads to the respi- 
ratory muscles. 

Treatment 

Antivenin is available, but only the specific antise- 
rum for the type of cobra involved should be used; 
victims are often tested for sensitivity before being 
treated. 

See also antivenin; snakes, poisonous. 



68 cobra, Indian 



cobra, Indian (Naja naja) Also known as the 
Asian cobra, this favorite of snalce charmers kills 
many thousands of people each year. It is com- 
monly found in paddy fields and urban areas 
of southern Asia, Indonesia, Taiwan, and the 
Philippines. In India, the species has a black-and- 
white spectaclelike mark on a very wide hood; 
in other locations, the Indian cobra has a ring 
or bar on its hood. Growing up to 6 feet long, 
it is generally inoffensive but highly aggressive 
when restrained; it is active at dusk and during 
the night. When confronted by an aggressor, it 
rears up the front of its body and inflates its hood, 
standing its ground. Its venom is highly neuro- 
toxic; it is fatal so often because it comes into 
populated areas to seek out rats. 

Symptoms 

Pain radiating from the wound, swelling, numb- 
ness, drooping eyehds, difficulty in speaking, weak- 
ness, respiratory distress, bhndness, convulsions, 
and death. 

Treatment 

Antivenin is available, but only the specific antise- 
rum for the type of cobra involved should be used; 
victims are often tested for sensitivity before being 
treated. 

See also antivenin; snakes, poisonous. 

cobra, king (Ophiophagus hannah or Naja hannah) 

The world's largest venomous snake, the king 
cobra (or hamadryad) is found in forests and areas 
of rural agriculture from southern China to the 
Philippines and Indonesia. This huge snake can 
grow as long as 18 feet; when angered, it raises its 
head and can stand as tall as a person. A normally 
quiet snake, the king cobra is highly dangerous 
when aroused; its bite is lethal about 10 percent of 
the time. It spreads a small hood, and while adult 
snakes have a dull color with no markings, young 
snakes sport a black skin with narrow chevrons of 
pale yellow on buff. 

King cobras are often found in pairs, which may 
be the origin of the ancient belief that a person 
who kills a king cobra will be pursued and killed 
by its mate, intent on revenge. 



King cobras are the most intelhgent and curious 
of snakes and in captivity will watch any activity 
going on outside their cage. They are rarely kept in 
zoos outside of the tropics, however, because they 
are selective feeders, existing entirely on other spe- 
cies of snakes. 

Symptoms 

Within 15 to 30 minutes symptoms appear: pain, 
swelling, a drop in blood pressure, and confusion 
followed by death if the poison spreads to the respi- 
ratory muscles. 

Treatment 

Antivenin is available, but only the specific antise- 
rum for the type of cobra involved should be used; 
victims are often tested for sensitivity before being 
treated. 

See also antivenin; snakes, poisonous. 

cobra, spitting (Naja nigricollis) This nervous and 
aggressive cobra is widely found throughout Africa, 
except in the extreme south and the Sahara. It is 
one of the cobras that can eject venom at a victim's 
eyes at distances of up to more than 7 feet; the 
venom can cause temporary or permanent bhnd- 
ness unless promptly washed out. Also called the 
black-necked cobra, this snake prefers to spit and 
rarely bites. The sprayed venom is harmless to 
unbroken skin. 

Symptoms 

The venom of a cobra snake is chemically different 
from the venom of other snakes. Within 15 to 30 
minutes symptoms appear: pain, swelling, a drop in 
blood pressure, and confusion followed by death if 
the poison spreads to the respiratory muscles. 

Treatment 

The specific antiserum for the type of cobra involved 
should be used, and victims are often tested for 
sensitivity before being treated. 

See also antivenin; snakes, poisonous. 



cocaine One of the most popular of the abused 
drugs in America today, cocaine is an alkaloid of 



cocaine 69 



the coca plant grown on the slopes of the Andes, 
where it has been cultivated for thousands of years. 
The oval leaves that provide cocaine and 1 3 other 
alkaloids are picked four times a year, and the 4- 
foot-high bushes continue to produce the leaves 
for up to 30 years. After the leaves are harvested, 
they are dried (sometimes in the sun or in a fire) 
and then packed for shipment. Cocaine has many 
uses as a medicine, and is especially valuable as 
a local anesthetic. As a solution of one of its acid 
salts, cocaine has long served as a topical anesthetic 
in the eye and on mucous membranes, but it is not 
commonly used in clinical medicine today. It is, 
however, still used in veterinary medicine. 

Indians throughout the Andes chew coca leaves 
at an early age and continue the habit through 
their lifetime. Cocaine was first extracted from 
the leaves of the coca bush in Germany more 
than 100 years ago, and the kick obtained from 
sniffing the white powder was soon recognized. 
Indeed, cocaine was enthusiastically recommended 
by many medical authorities, including Sigmund 
Freud, who believed it could cure alcoholism 
and promote sexuahty. Sir Arthur Conan Doyle, 
another cocaine adherent, popularized it further by 
making his character Sherlock Homes a sniffer and 
needle abuser of the white powder. 

In the United States, a soft drink developed in 
1886 by an Atlanta druggist contained a touch of 
cocaine and caffeine from the African cola nut, 
becoming famous as Coca-Cola; under pressure 
from the U.S. government in 1903, however, all 
cocaine was removed from the beverage. Coke's 
removal of the drug kicked off a federal crack- 
down on the use of cocaine, and beginning in 
1906 a series of laws placed it under strict federal 
regulation. 

Cocaine may be sniffed ("snorted"), smoked, 
or injected; combined with heroin and injected, 
it is called a "speedball." Addicts prefer to inject it 
intravenously for the brief but intense elation that 
it induces. Similar to amphetamine in some of its 
action, cocaine even in a large oral dose dissipates 
quickly (usually within two to three hours). 

"Crack" (the "freebase" form of cocaine) is made 
by dissolving cocaine salt in solution and extract- 
ing the freebase form with a solvent, such as ether. 
Heat is often applied to hasten solvent evapora- 



tion. Cocaine sold as a street drug may also con- 
tain caffeine, phenylpropanolamine, ephedrine, or 
phencyclidine. 

Cocaine is a local anesthetic and a central ner- 
vous system stimulant, with an intoxication resem- 
bling an amphetamine "high." It is well absorbed 
in the body, and smoking or injections can produce 
the maximum effects within a few minutes. Oral 
or nasal application may take up to 30 minutes. 
Its toxicity varies greatly from one individual to 
the next and is also affected by the presence of 
other drugs in the system. Still, the oral lethal dose 
is described as about 1 gram in adults, but some 
addicts are reported to have consumed as much as 
10 grams in one day, reflecting an acquired toler- 
ance. The method of use also affects toxicity; inject- 
ing or smoking cocaine may produce such rapid 
high levels in the brain or heart that convulsions 
or heart attack may occur, while the same dose 
ingested or snorted may produce only a feehng of 
euphoria. 

Symptoms 

Cocaine can be toxic to both the central nervous and 
the cardiovascular systems. Symptoms include anx- 
iety, agitation, delirium, psychosis, muscle rigidity, 
hyperactivity, seizures, and coma. Chronic cocaine 
use causes weight loss, insomnia, and paranoid 
psychosis. In addition, symptoms may include fatal 
heart irregularities, severe hypertension, stroke, 
coronary artery spasm, heart attack, chronic heart 
disease, shock, and kidney failure. Death is usually 
caused by a sudden fatal heart irregularity, seizure, 
brain hemorrhage, or multiple organ failure. Other 
symptoms can occur from snorting or smoking 
cocaine, including chest pain, nasal septal perfora- 
tion, and skin ulcers ("coke burns"). 

Treatment 

There is no specific antidote. Provide symptomatic 
treatment; after cocaine ingestion, perform gastric 
lavage but do not induce vomiting because of the 
risk of seizures. Administer activated charcoal and a 
cathartic. For those who have ingested large pack- 
ets of cocaine in an attempt to smuggle or hide the 
drug, give repeated doses of activated charcoal and 
consider whole gut lavage (otherwise, laparotomy 
and surgical removal may be necessary). 



70 codeine 



codeine (methylmorphine) This narcotic pain- 
killer is a naturally occurring alkaloid of opium 
(from the poppy plant) used in medicine as a cough 
suppressant and narcotic analgesic drug. It was 
first synthesized from morphine (an opium deriva- 
tive) in 1832; although it can be extracted directly 
from opium, most of the codeine used in drugs is 
produced from morphine. When taken over a long 
period of time, codeine may be habit-forming. 

Supertoxic, it is used to treat mild to moderate 
pain and can also be used as an antidiarrheal. It is 
found in combination with a wide range of other 
drugs, such as acetaminophen, aspirin, caffeine, 
and cough suppressants. Because of its value as a 
cough suppressant, it had been included in a num- 
ber of cough medicines in the past. But because 
they were available to those who experimented 
with drugs, codeine was removed from many of 
these products. However, more than 40 prescrip- 
tion cough medicines still contain codeine. 

Nearly transparent, it has no odor and a bit- 
ter taste and is sold as either a powder or liquid. 
In some forms it is a Schedule II drug (a strictly 
controlled drug considered by law to have a high 
potential for abuse), and psychological dependence 
can develop fairly rapidly, but it is not a major drug 
of abuse. 

Symptoms 

Within 20 minutes after ingestion, victims will 
begin to feel sleepy, giddy, and clumsy, with a 
slow heartbeat; overdoses can lead to excitability, 
breathing problems, coma, and death. 

Treatment 

Naloxone is the antidote; other symptoms are 
treated as they appear. 

See also alkaloids; naloxone. 

Cogentin See benztropine. 

coliform bacteria The common microorganism 
Escherichia coli (or E. coli) that is found in the 
intestines of humans and other animals; in the 
gut the bacteria do not cause disease, but a high 
concentration of the bacteria in drinking water 



supplies or aquatic ecosystems is often an indicator 
of pollution. 

colocynth (Citrullus colocynthis) Also known as 
bitter apple or bitter cucumber, this extremely toxic 
bitter fruit is native to the Mediterranean but can 
also be found in Central America. 

Poisonous part 

The toxic fruit contains colocynthin, which is used 
as an insecticide, purgative, and abortifacient. 

Symptoms 

Within several hours of ingestion, symptoms of 
bloody diarrhea appear, followed by cramps, head- 
ache, kidney failure, and death. Those who live 
more than two days will most likely recover. 

Treatment 

Administer milk to relieve stomach irritation and 
atropine to minimize gastric secretions, plus medi- 
cation for pain. 

comfrey (Symphytum officianale) [Other names: 
gum plant, healing herb, knitbone, nipbone.] Once 
a popular tea herb found in every herbalist's gar- 
den and used to aid digestion and promote heahng, 
comfrey has been shown to be poisonous by recent 
studies, although the findings are considered by 
some to be controversial. 

Naturalized throughout North America and 
native to Europe and Asia, comfrey is a hardy 
perennial with a stout, brown-black root (from 
which the plant gets its nickname, "slippery root") 
and blue, yellow, white, or red tubular flowers 
appearing in May and June. It grows to about 3 
feet high and has coarse, hairy egg-shaped leaves; 
its fruit of black nuts can be seen in August. It is 
found along stream banks and in rich soils of moist 
meadows. 

As early as 400 B.C. comfrey was used to stop 
heavy bleeding and to treat bronchial problems. Its 
popularity as a treatment for broken bones gave 
the plant its name, a derivative from the Latin con- 
ferta ("to grow together"). In the 1 9th century dur- 
ing the Irish potato famines, the plant was seen as 



cone shell 71 



a solution to world hunger by Englishman Henry 
Doubleday, who founded an association still in 
existence today to promote the plant's use. 

While remedies derived from the roots have 
been prescribed since the early 1500s for every- 
thing from tumors to burns and gangrene, in 
the early 1970s darker reports about this herb's 
character began to surface: a weed containing pyr- 
rolizidine alkaloids fell into some wheat being har- 
vested in Afghanistan. When the farmers and their 
families ate the bread made from the contaminated 
wheat, 25 percent of the 7,200 villagers developed 
liver ailments within two years. 

Poisonous part 

Recent studies show the roots and leaves of all 
varieties contain potentially dangerous compounds 
called pyrrolizidine alkaloids, which have caused 
liver tumors in animals. While comfrey leaves 
(from which tea is brewed) have only one-tenth 
the alkaloid concentration as the root, several teas 
on the market contain both root and leaves. In 
other comfrey products, such as comfrey-pepsin 
tablets (called "digestive aids"), comfrey root is a 
primary ingredient. 

Symptoms 

In 1976 and 1985 there were two cases of pyr- 
rolizidine-alkaloid poisoning in humans, probably 
from drinking comfrey tea. One recent study found 
that rats fed a diet that was 8 percent comfrey 
developed liver cancers within six months; another 
showed that certain alkaloids in comfrey cause 
chronic liver problems in rats. 

Treatment 

Physicians suggest that since comfrey tea won't 
cure illness and may damage the liver, it is wise to 
avoid this herb until researchers perfect an accu- 
rate test for alkaloid levels in comfrey leaves. 
See also herbs, unsafe. 

compound 1080 Also known as sodium fluoro- 
acetate and used as a rat poison, this is one of the 
most toxic substances known; fluoroacetic acid is 
no longer sold in the United States because of its 
danger, but fluoroacetate is still available. 



Fluoroacetate blocks cell metabolism, and as 
little as I mg is enough to cause serious symptoms. 
The effects of fluoroacetate poisoning are similar to 
those of cyanide and hydrogen sulfide, although 
they take longer to develop. 

Symptoms 

Within a few minutes to several hours after inges- 
tion, symptoms appear, including nausea, vomiting, 
diarrhea, metabolic acidosis, agitation, confusion, 
seizures, coma, respiratory arrest, and heartbeat 
irregularities. Death results from respiratory failure 
due to pulmonary edema or ventricular fibrillation. 

Treatment 

There is no antidote. Perform gastric lavage but 
do not induce vomiting, since seizures may occur 
as early as 30 minutes after ingestion. Administer 
activated charcoal and a cathartic. 
See also cyanide; hydrogen sulfide. 

cone shell (Conus) These highly toxic stinging 
shells are found on or around coral reefs in warm 
waters, and although prized by collectors for their 
bright, spotted shells, they have caused several 
human deaths. Cone shells are tiny (only one to 
three inches long) members of the enormous mol- 
lusk family, with a cone-shaped shell with wavy 
stripes or an irregular pattern. The more than 70 
different species in this family of toxic marine 
snails can fire a barbed harpoonhke device from a 
slit in their shell to obtain food and protect against 
predators. 

There are three main types of cones — those that 
eat worms, mollusks, or fish. Of all the cones, the 
fish-eating varieties are most dangerous to humans; 
they have teeth strong enough to pierce cloth. 

Cones live in warm waters of barrier reefs in 
the Indo-Pacific, Australia and the Mediterranean, 
southern California and New Zealand. Some of 
the most common include the geography cone (C. 
geographus), striated cone (C. striatus), and the tulip 
cone (C. tulipa). 

Poisonous part 

The cone shell uses its sting to secrete a neurotoxin 
that competes for acetylcholine in the body, and 
can be fatal within 15 minutes. 



72 coniine 



Symptoms 

Pain, swelling, numbness or tingling, dizziness, 
blurred vision, difficulty swallowing, weakness, 
ataxia, breathing problems, paralysis, coma, and 
death. 

Treatment 

There is no known antidote. Contact medical help 
immediately; flush the wound with fresh- or salt 
water, and then soak the affected area in hot water 
or put hot compresses on it. The water should be 
very hot (122°F), so that the heat will deactivate 
the poison. Continue applying hot water for 30 
minutes to an hour. Have the victim lie still with 
the stung part immobile and lower than the heart. 
Tie a flat strip of cloth around the stung arm or leg 
two to four inches above the sting. It should be 
snug but loose enough to allow a pulse farther out 
on the limb. Check periodically and loosen if neces- 
sary, but do not remove it. If swelling reaches the 
band, tie another band two to four inches higher 
up and remove the first one. Generally, victims 
recover within 48 hours. 



coniine The most important of the six alkaloids 
found in all parts of Conium maculatum (poison 
hemlock), a plant widely found throughout the 
United States and Europe. The whole plant exudes 
a foul odor (similar to cat urine or mice) at least in 
part attributable to the volatile coniine. Prolonged 
inhalation of the odors is said to cause a narcosis. 
The toxic potential of coniine has been known 
since earliest times and was presumably instru- 
mental in the death of Socrates. 

See also alkaloids; hemlock, poison. 

copperhead, Australian (Denisonia superba) A 

poisonous snake of the cobra family found in Tas- 
mania and along the coasts of southern Australia. 
About 5 feet long, this copperhead is usually cop- 
per or reddish brown. Although dangerous, it is 
unaggressive when not disturbed. 

Symptoms 

The venom of a cobra snake is a toxin chemically 
different from that of other snakes; some suggest 



it may contain a cardiotoxin. Within 15 to 30 
minutes symptoms appear: pain, swelling, a drop 
in blood pressure, confusion, slurring of speech, 
dilation of the pupils, strabismus (abnormal devia- 
tion of one eye in relation to the other), drooping 
of the upper eyelid, and muscle weakness. The 
respiratory muscles are affected last, and respira- 
tory muscle paralysis is the most common cause 
of death. 

Treatment 

Antivenin is available, but only the specific antise- 
rum for the type of cobra involved should be used; 
victims are often tested for sensitivity before being 
treated. 

See also antivenin; snakes, poisonous. 

copperhead snake (Agkistrodon contortrix) Also 
called highland moccasin, this species of copper- 
head is a member of the Viperidae family and one 
of several unrelated snakes that get their name 
from the reddish color of the head. The Agkistro- 
don variety is the North American copperhead, a 
venomous species found in swampy, rocky, and 
wooden regions of the eastern and central United 
States. It is considered a pit viper because of the 
characteristic small sensory pit between each eye 
and nostril. 

Usually less than three feet long, the copperhead 
is a pink or red snake with a copper-colored head 
with reddish brown hourglass-shaped crossbands 
on its back. While many bites are reported, the 
venom of this snake is relatively weak and rarely 
fatal. The copperhead has retractable hollow fangs 
in the front of the upper jaw that can be folded 
back and then positioned forward as the mouth 
opens to strike. 

Seriousness of the bite depends on a wide 
variety of variables, including the snake's size 
(usually the larger, the more venomous) and 
whether the snake is hungry or alert. The angle 
of the bite and its depth and length also affect the 
seriousness of the bite. In addition, the victim's 
size (children and infants are at greater risk) and 
health at the time of the bite will also affect the 
outcome. People with diabetes, hypertension, or 
blood coagulation problems and the elderly are 



coral plant 73 



particularly sensitive to snake venom, and men- 
struating women may bleed excessively following 
the bite of a pit viper. Several cases of miscarriage 
have been reported when pregnant women have 
been bitten. 

Finally, the location of the bite itself is crucial to 
its severity; venomous snake bites on the head and 
trunk are twice as serious as those on the extremi- 
ties, and bites on the arms are more serious than 
those on the legs. 

Poisonous part 

The venom is a mixture of proteins that acts on 
a victim's blood, and even snakes that appear 
to have been killed by the side of the road have 
been reported to bite. The size of the snake can 
give an idea of its potential dangerousness and 
can be judged by the distance between the fang 
marks. Fang marks less than eight millimeters 
apart suggests a small snake; eight to 12 millime- 
ters indicates a medium-size snake and more than 
12 mm suggests a large venomous snake. Even 
snakes that have been "defanged" can be danger- 
ous, since all snakes grow new fangs from time 
to time. 

Symptoms 

Swelling, internal bleeding, and changes in red 
blood cells; central nervous system symptoms 
include convulsions and sometimes psychotic 
behavior, muscle weakness, and paralysis. In addi- 
tion, there are general systemic symptoms of fever, 
nausea, vomiting, diarrhea, pain, and restlessness. 
Slow or rapid heartbeat can develop, and kidney 
failure has been reported. 

Treatment 

Within the first 30 to 45 minutes after the bite, 
apply a venous tourniquet a few inches above 
the bite, loosening it every 15 to 30 minutes 
and reapplying it above the level of progressive 
swelling. Keep the victim quiet, lying down to 
decrease metabolic activity (which affects the 
spread of the venom). The wound area (especially 
if it is an arm or leg) should be kept lower than 
the heart. Within 30 minutes, trained individu- 
als can incise the wound area and apply suction. 
Antivenin is available but should be administered 



within four hours; antivenin is rarely helpful if 
given more than 12 hours after the bite. Tetanus 
prophylaxis is advisable; other treatment might 
include blood transfusions, intravenous fluids, 
treatment for convulsions, and antihistamines 
to control itching. In addition, broad-spectrum 
antibiotics may be administered, since snakebites 
are notorious for becoming infected. If antivenin 
has not been administered (or was given hours 
after the bite), sloughing of the skin around the 
bite is common. 

See also antivenin; pit viper; snake, poisonous. 

coprine A water-soluble substance found in the 
wild mushroom Coprinus atramentarius and a few 
other less common species of the same genus. Its 
metabolites inhibit the liver enzyme acetaldehyde 
dehydrogenase. If even small amounts of ethanol 
(alcohol) are consumed within several days after 
eating the mushroom, acetaldehyde accumulates 
in the blood, causing illness. In the absence of 
alcohol, however, C. atramentarius is a safe, edible 
mushroom. 

See also inky cap; mushroom poisoning. 

coral plant (Jatropha multifida) This plant is so 
poisonous that even a small amount — ^just one 
seed — can be toxic for a small child. This large, 
attractive plant is often kept as a houseplant 
despite its toxicity. It has large, deeply lobed circu- 
lar leaves and coral-red flowers that bloom most 
of the year, and its yellow fruit has one seed in 
each of its three sides. It is a member of a large 
genus of shrubs or small trees with a three-sided 
seed capsule, found throughout the Western 
Hemisphere. 

Poisonous part 

Seeds and perhaps other parts of the plant contain 
the poison jatrophin, which interferes with protein 
synthesis in the intestinal wall. The coral plant also 
contains a plant lectin (toxalbumin) and cathartic 
oils that are toxic. Ingestion of just one seed can be 
serious. The plant lectin inhibits protein synthesis 
in cells of the intestinal wall and may cause serious 
or fatal poisoning. 



74 coral poisoning 



Symptoms 

The onset of symptoms (nausea, vomiting, and 
diarrhea) occurs rapidly, unlike poisoning with 
other plants with toxic lectins. 

Treatment 

Give fluids and provide supportive treatment. 
See also Barbados nut; bellyache bush. 

coral poisoning A cut from a coral reef may 
seem innocuous and is often ignored by visitors to 
the temperate waters where coral reefs are found. 
Because coral abrasions always contain pieces of 
animal protein and bits of coral material, even the 
slightest scratch may become infected, turning into 
a nasty ulcer that recurs for many years. 

In addition to the true corals, there is also a 
"hydroid" coral, or stinging coral (also called fire 
coral), which is important to the formation of reefs. 
Its exoskeleton is made up of calcium carbonate, 
which is covered with tiny pores and is found off 
the Florida Keys and in the Caribbean. 

Symptoms 

Immediately after coming in contact with the coral, 
the victim exhibits welts, itching, and burning at 
the wound site. The wound may weep and form 
wheals. Stinging coral causes burning pain on 
contact. 

Untreated, a coral cut — which looks innocuous 
enough at first — can within days become an ulcer 
that continuously sloughs off and is surrounded 
by a painful swelling. This ulcer can be incredibly 
painful — much more so than it looks — and can be 
quite disabling. If the wound is on the legs, the vic- 
tim may be unable to walk for months. Generalized 
symptoms can include enlargement of local lymph 
glands, fever, and malaise. Relapses are common 
and occur without warning. 

Fire coral scrapes often result in bleeding that 
helps remove the toxin but may be severe enough 
to require direct pressure on the wound to control 
blood loss. 

Treatment 

Ideally, antiseptics should be applied as soon as a 
person gets the smallest coral cut. Cleanse with 



soap and water, dry and clean with alcohol, dry 
again, and rinse with hydrogen peroxide. In severe 
cases, the person should be put to bed with the 
wound elevated and given kaolin poultices, antibi- 
otics, and antihistamines. 



coral snake There are about 65 species of this 
strongly patterned snake, a member of the cobra 
family — and all are dangerous. While true coral 
snakes are found primarily in the tropics, similar 
forms can also be found in Asia and Africa. In 
addition, there are two varieties of coral snakes 
found in the United States, the only species of 
Elapidae that are native here. They are the eastern 
coral snake (Micrurus fulvius) and the Arizona coral 
(Micruroides euryxanthus euryxanthus) . Although 
coral snakes rarely bite when handled, the venom 
of some of them is capable of killing a person. The 
largest genus (Micrurus) ranges from the southern 
United States to Argentina. Other coral snakes 
include the African coral (Aspidelaps lubricus); the 
black-banded coral (Micrurus nigrocinctus) found 
in Central America; and the often-fatal Brazilian 
giant coral (M. frontalis), found in southern South 
America. 

Poisonous part 

Strikingly colored, coral snakes have alternating 
red and black bands separated by narrow yellow 
or white rings. Their grooved fangs are fixed to the 
front part of the upper jaw and cannot be folded 
back, unlike the vipers and pit vipers. This is one of 
the snakes for which an old rhyme can sometimes 
be useful to differentiate poisonous from nonlethal 
varieties. Old folk rhymes hold that it is possible 
to tell the difference between harmless and deadly 
coral snakes by the stripes — deadly varieties have 
red stripes next to yellow ones. There are several 
versions of these rhymes: "Red on yellow, kill a 
fellow; red on black, okay Jack" or "Red touching 
yellow, dangerous fellow." 

Symptoms 

Numbness at bite, headache, facial swelling, sore 
throat, skin hypersensitivity, drooping eyelids, 
photophobia, vomiting, rapid heartbeat, backache, 
irritability, and death. Some species of coral snakes 



coral snake, eastern 75 



have a venom that breaks down the red blood cells 
and frees the hemoglobin, which then appears in 
urine. 

Treatment 

Antiserum is available for some species, but not 
for all. There is antivenin for the eastern coral 
snake; there is no antivenin for the Arizona coral 
snake. 

See also antivenin; antivenin, coral snake; 

SNAKES, POISONOUS. 

coral snake, Arizona (Micruroides euryxanthus 
euryxanthus) Also known as the Sonoran coral, 
this is one of two coral snake species found in the 
United States. A rare variety of coral snake, it has 
a potent bite but rarely strikes humans. Found 
in the southwestern United States deserts, it is 
quite small and rarely seen, coming out from its 
underground retreat only at night — usually after 
a warm rain. When disturbed, it buries its head 
in its coils and raises and exposes the bottom of 
its tail. 

Several harmless snakes look very similar in 
color to the coral snakes, and it is important to 
be able to tell the difference. The Arizona coral 
has wide red and black bands separated by yellow 
rings, all almost the same width. 

Poisonous part 

The venom of the coral snakes contains a deadly 
neurotoxin that can be fatal and is beheved to 
block the uptake of acetylchohne at the receptor 
sites. Their small, nonmovable fangs are not as 
efficient as those of vipers, and so this snake must 
hold on to its victim for a longer period of time in 
order to inject its venom. 

Symptoms 

Symptoms appear within one to five hours, 
although occasionally it takes even longer. Early 
signs are systemic and include slurring of speech, 
dilation of the pupils, strabismus (eye movement), 
drooping of the upper eyehd, and muscle weak- 
ness. The respiratory muscles are affected last, and 
respiratory muscle paralysis is the most common 
cause of death in coral snakebites. 



Treatment 

Antivenin is available; should it be inaccessible, 
it may be possible to maintain life by intensive 
life support measures through the period of 
acute respiratory muscle paralysis. The poison is 
metabolized after about four days, symptoms fade 
and recovery is usually complete in those who 
survive. 



coral snake, eastern (Micrurus fulvius) Also 
called a harlequin snake, this fairly small non- 
hooded member of the cobra family is found in 
North Carolina and Missouri to northeastern 
Mexico in moist, dense vegetation near ponds or 
streams and in hardwood forests, pine flats, rocky 
hillsides, and canyons. While common, this noc- 
turnal snake is rarely seen and prefers burrowing 
at night. 

About 30 inches long, the eastern coral snake 
has wide bands of red and black separated by 
narrow yellow rings, and the head is completely 
black from the end of its blunt nose to just behind 
the eyes. The red rings are sometimes spotted 
with black. The eastern coral can be confused 
with the harmless scarlet snake and the scarlet 
king snake. 

One of the few snakes that make a warning 
noise as they strike, the eastern coral has been 
heard to produce a succession of popping noises by 
drawing air at its vent and then expelling it. 

Symptoms 

The bite of the eastern coral snake is unlikely to 
be fatal unless there is a prodigious amount of 
venom or the bite is in a particularly vulnerable 
place. Symptoms appear within one to five hours, 
although occasionally it takes longer. Early signs 
are systemic and include slurring of speech, dila- 
tion of the pupils, strabismus (abnormal deviation 
of one eye in relation to the other), drooping of the 
upper eyelid, and muscle weakness. The respira- 
tory muscles are affected last. 

Treatment 

Antivenin is available. 

See also antivenin; antivenin, coral snake; 

SNAKES, poisonous. 



76 corn cockle 



corn cockle (Agrostemma githago) Native to 
Europe but introduced in America, the annual is 
tall and gray, with purple pin petals and pink flow- 
ers, and is occasionally grown as an ornamental. 
The milled seeds of this noxious weed may be 
found in flour. 

Poisonous part 

The entire plant is poisonous (active ingredient is 
githagin and saponin glycosides), but the seeds are 
particularly deadly — especially if ground up with 
flour or cereal. 

Symptoms 

Frequent ingestion of small amounts causes a 
chronic disease resulting in pain, prickhng and 
burning of the lower extremities, and increasing 
paralysis. Symptoms may appear within 30 minutes 
to an hour after ingestion and include dizziness, 
diarrhea, respiratory distress, vomiting, headache, 
sharp pain in the spine, coma, and death. 

Treatment 

Gastric lavage and treatment of symptoms. 

corticosteroids Used principally as an anti- 
inflammatory agent, these drugs are used to treat 
arthritis, bursitis, certain skin diseases, adrenal 
gland insufficiency, thyroiditis, some cancers, 
asthma, and other disorders. Though normally not 
highly toxic, they pose a serious danger to those 
with allergies or gastrointestinal tract disease, pep- 
tic ulcers, or poor heart function. Treatment is the 
same as that for general anti-inflammatory drugs. 
See also anti-inflammatory drugs. 



cortinarius mushrooms The members of the Cor- 
tinarius genus of mushrooms, once thought to be 
harmless, are deadly poison — almost as poisonous 
as the Amanita genus of mushrooms. A little more 
than a cup of the cooked mushrooms can be fatal. 
Found in central Europe, the mushrooms have 
caps ranging from blue violet (which can be eaten) 
to those of brown or red (deadly); they get their 
name from the veil that sometimes covers the gills 
of young mushrooms. 



Poisonous part 

The mushroom contains the poison orellanin, 
which damages the liver and kidneys. 

Symptoms 

Symptoms do not appear until three days to two 
weeks after ingestion; by then, the victim develops 
excessive thirst and may drink several liters of fluid 
a day. By this time, the liver and kidneys usually 
have been irreversibly damaged. Other symptoms 
may include nausea, headache, muscular pains, 
and chills. 

Treatment 

Gastric lavage, if performed immediately after 
ingestion. In general, the only treatment once 
symptoms appear are kidney and liver trans- 
plants. 

See also mushroom poisoning; mushroom 

TOXINS. 

cottonmouth snake See water moccasin. 



Coyotillo (Karwinskia humboldtiana) A small tree 
or shrub that grows in Texas, New Mexico, and 
Mexico, and reaches a height of up to 24 feet. Its 
small green flowers bloom during the summer, and 
its black to brown fruit matures around October. 
The plant is toxic to humans as well as to cattle, 
hogs, goats, sheep, and fowl. 

Poisonous part 

The leaves and fruit are poisonous and contain 
polyphenolic compounds. 

Symptoms 

Chronic ingestion may cause ascending paral- 
ysis; weakness occurs after a latent period of 
several weeks; paralysis may progress for a 
month or more. The neurological picture is simi- 
lar to that of Guillain-Barre syndrome or other 
polyradiculoneuropathies. 

Treatment 

Supportive. If victims survive respiratory paralysis, 
they will recover completely. 



creosote 77 



crack cocaine See cocaine. 



creosote Creosote is the name used for a variety of 
products that are mixtures of many chemicals; those 
products include wood creosote, coal tar creosote, 
coal tar, and coal tar pitch. Creosotes don't occur 
naturally in the environment; they are created by 
high-temperature treatment of woods (wood creo- 
sote) or coal (coal tar creosote), or from the resin of 
the creosote bush (creosote bush resin). 

Coal tar creosote is the most common form of 
creosote in the workplace and at hazardous waste 
sites in the United States; it is referred to by the 
U.S. Environmental Protection Agency (EPA) as 
"creosote." This thick, oily liquid is typically amber 
to black in color and is a distillation product of coal 
tar. It has a burning, caustic taste. Coal tar creosote 
is the most widely used wood preservative in the 
United States; it is apphed to preserve and water- 
proof wood for log homes, railroad ties, telephone 
poles, marine pilings, and fence posts. It's also a 
restricted-use pesticide and is used as an animal 
and bird repellant, insecticide, animal dip, fungi- 
cide, and pharmaceutical agent for the treatment 
of psoriasis. About 300 chemicals have been identi- 
fied in coal tar creosote, but there may be as many 
as 10,000 other chemicals in the mixture. 

Wood creosote ranges in color from clear to yel- 
low; it's a greasy liquid with a characteristic smoky 
odor and sharp burned taste. The major chemicals 
in wood creosote are phenol, cresols, and guaiacol. 
This type of creosote has been used as a disinfec- 
tant, a laxative, and a cough treatment; it is rarely 
used today in the United States but is still used as 
an expectorant and a laxative in Japan. 

Coal tar and coal tar pitch are the by-products 
of the high-temperature treatment of coal to make 
coke or natural gas; they are usually thick, black 
or dark brown hquids or semisolids with a naph- 
thalene-like odor. Coal tar products, which have 
a sharp, burning taste, are found as ingredients in 
medicines used to treat skin diseases such as psoria- 
sis and in insecticides, animal dips, and fungicides. 

Coal tar creosotes, coal tar, and coal tar pitch 
are similar in composition; the major chemicals 
in them that can cause harmful health effects are 
polycychc aromatic hydrocarbons, phenol, and cre- 



sols. Creosotes and coal tars are complex mixtures 
that contain primarily condensed aromatic ring 
compounds or phenols. 

Coal tar creosote components dissolved into 
water move through the soil to eventually reach 
and enter groundwater, where they may per- 
sist; once in the water, biodegradation may take 
months. Biodegradation in soil can take months 
for some components of coal tar creosote, or much 
longer for others. 

No federal criteria have been set for creosote lev- 
els in water, and there are no air standards. In 1978, 
the EPA initiated a special review of creosote based 
on its cancer- causing reputation; as a result, it did 
not ban the substance but proposed a set of regula- 
tions intended to reduce exposure. Creosote is listed 
as a hazardous air pollutant in the 1990 Clean Air 
Act, requiring the EPA to set emission standards 
and is on the EPA community right-to-know list. 
Creosote is also a restricted-use pesticide, meaning 
that it may be applied only by certified applicators. 

The Consumer Awareness Program recommends 
against using creosote-treated wood products in 
proximity to food, animal food, and public drink- 
ing water. People are advised not to burn creosote- 
treated wood, and apphcators must wear protective 
clothing, special face masks or goggles, respirators, 
and gloves. If creosote is used on wood that will 
touch bare skin (such as in playground furniture 
or outdoor furniture), two coats of urethane or 
shellac sealer must be applied. A sealer should also 
be applied to treated wood used in areas where 
inhalation exposure may occur, such as in barns 
and stables. 

Symptoms 

The International Agency for Research on Cancer 
and the EPA have determined that coal tar creosote 
probably causes cancer in humans. The EPA has 
determined that coal tar pitch is a human carcino- 
gen; it classified coal tar creosote as a carcinogen in 
the 1992 Toxic Release Inventory (TRI). 

Cancers of the skin and scrotum have been 
hnked to long-term exposure to low levels of 
these chemical mixtures, especially through direct 
contact with skin during wood treatment or 
manufacture of coal tar creosote-treated products, 
or in coke or natural gas factories. Cancer of the 



78 crocus 



scrotum in chimney sweeps has been associated 
particularly with prolonged skin exposure to soot 
and coal tar creosote. 

Eating food or drinking water contaminated 
with a high level of creosotes may cause burning 
in the mouth and throat, as well as stomach pains. 
Brief exposure to large amounts of coal tar creosote 
may result in a rash or severe irritation of the skin, 
chemical burns of the surfaces of the eye, convul- 
sions, mental confusion, kidney or liver problems, 
unconsciousness, or even death. 

Longer exposure to lower levels of coal tar 
creosote, coal tar, or coal tar pitch by direct contact 
with skin or by exposure to the vapors from these 
mixtures can also result in sun sensitivity and 
cause damage to skin, such as reddening, blistering, 
or peeling. Longer exposures to the vapors of the 
creosotes, coal tar, or coal tar pitch can also cause 
irritation of the respiratory tract. 

Treatment 

If the victim is alert, give a slurry of activated char- 
coal and perform careful gastric lavage if there are 
no deep burns in the mouth or pharynx. AVOID 
ADMINISTRATION OF ALCOHOL. Remove con- 
taminated clothing, and blot up liquid on skin 
(caregiver should wear gloves). Wash exposed 
areas of the skin, and give morphine for pain. 
Sodium bicarbonate may ease symptoms; give oxy- 
gen as needed and monitor vital signs. 
See also phenol. 



crocus See meadow saffron. 



croton (Croton tiglium) Also known as mayapple, 
this supertoxic plant is native to Southeast Asia and 
now also grows in the southwestern United States. 
Croton oil in alcohol is also known as a "Mickey 
Finn." 

Poisonous part 

Seeds and extracted oil from the plant are deadly. 

Symptoms 

Skin contact results in immediate blistering and 
irritation, which can last up to three weeks. If the 



seeds or oil are ingested, symptoms appear within 
10 to 15 minutes and include burning pain in the 
mouth and stomach, bloody diarrhea, kidney and 
liver damage, nausea, vomiting, fast heartbeat, 
coma, and death. 

Treatment 

Vomiting and gastric lavage are ineffective. Give 
fluids orally along with intravenous infusion to 
correct electrolyte imbalance; treat symptoms. 

cryptosporidiosis One of the more recently dis- 
covered types of food poisoning, cryptosporidi- 
osis is a reportable disease caused by a protozoan 
called Cryptosporidium parvum. The invisible microbe 
infects cells hning the intestinal tract; it was not 
identified as a cause of human disease until 1976. 

In 1993, a waterborne outbreak in Milwaukee 
sickened about 400,000 people. Parvum has been 
associated with diarrhea outbreaks in child-care 
centers throughout the country. In 1994, 302 
cases were reported to the New York state health 
department. 

Today it is a major threat to the U.S. water sup- 
ply. Able to infect with as few as 30 oocysts, Cryp- 
tosporidium has been found in untreated surface 
water as well as in swimming pools, wading pools, 
hot tubs, ice cubes, fruits and vegetables, lakes, riv- 
ers, day-care centers, and hospitals. 

Experts estimate that 2 percent of the population 
in North America is infected and that 80 percent of 
the population has had an infection in the past. In 
the United States, many outbreaks are never iden- 
tified, and the number of cases that occur each year 
aren't well documented. Some immunity follows 
infection, but the degree to which this immunity 
occurs is not clear. 

This parasite lives its entire life within the intes- 
tinal cells; it produces worms that are excreted in 
feces. These infectious worms can survive outside 
the human body for long periods of time, passing 
into food and drinking water, onto objects, and 
spread from hand to mouth. 

Because it is transmitted by the fecal-oral route, 
the greatest risk occurs in those infected people 
who have diarrhea, those with poor personal 
hygiene, and diapered children. It's also found 



curare 79 



in contaminated water, vegetables fertilized with 
manure, unpasteurized milk, or any food touched 
by an infected food handler. 

Symptoms 

Between one and 12 days after infection, victims 
experience watery diarrhea together with stomach 
cramps, nausea and vomiting, fever, headache, and 
loss of appetite. However, some people with the 
infection don't experience any symptoms at all. 
Healthy patients usually suffer with symptoms for 
only about two weeks. 

Diagnosis 

The infection is diagnosed by identifying the para- 
site during examination of the stool. If crypto- 
sporidiosis is suspected, a specific lab test should 
be requested, since most labs don't yet routinely 
perform the necessary tests. 

Treatment 

The Food and Drug Administration has approved 
nitazoxanide for treatment of diarrhea caused 
by Cryptosporidium in people who have a healthy 
immune system. Most people who have a healthy 
immune system will recover from the infection 
without treatment. Affected individuals should 
drink plenty of fluids to prevent dehydration. 
Young children and pregnant women may be more 
susceptible to dehydration, and rapid loss of fluids 
from diarrhea may be life-threatening to infants. 
People who have a compromised immune system 
are at greater risk for more severe and prolonged 
illness. The effectiveness of nitazoxanide is not cer- 
tain in this population. 

Complications 

People with an impaired immune system may have 
a severe and lasting illness; the resulting chronic 
diarrhea in this group may be fatal. Invasion of the 
lungs in these patients also may be fatal. 

Prevention 

Unfortunately, chlorine does not kill the proto- 
zoan; drinking water must be filtered to ehminate 
it. Many municipal water supplies do not have the 
technology to provide this filter. To prevent fur- 
ther transmission, hands should be washed often 



before and during food preparation, especially after 
changing diapers or working around young chil- 
dren. Infected people should not prepare any food 
that will be eaten raw. Fruits and vegetables should 
be thoroughly washed before eating. Cattle are a 
source of infection, so consumers shouldn't drink 
unpasteurized milk or untreated, unfiltered water 
in other countries. 



cube jellies See jellyfish. 

curare (Strychnos) A centuries-old extract from 
the bark and juices of trees in Central America 
(Strychnos toxifera), it has been used as a poison 
for arrows and for blowgun darts in Central and 
South America. Curare is a skeletal-muscle relax- 
ant drug, one of the alkaloid family of organic 
compounds. 

It is used in medicine today as an auxiliary to 
general anesthesia (frequently with cyclopropane), 
especially in abdominal surgery. Curare acts as a 
neuromuscular blocking agent that produces flac- 
cidity in striated muscle. Used by South American 
Indians against enemies and animals, curare is now 
widely available in the United States as a drug, 
where it is used to stop normal breathing and allow 
the patient to be placed on a respirator in order to 
treat the lungs. 

Poisonous part 

All parts of the 5. toxifera plant contain tubocurarine, 
a drug that interferes with muscle contractions by 
interfering with the action of the neurotransmitter 
acetylcholine. Curare is harmless if swallowed. Its 
poison is activated only if injected or administered 
intravenously. 

Symptoms 

Almost immediately, curare affects the muscles of 
the toes, ears, and eyes, then those of the neck and 
limbs followed by muscles important for breathing. 
Death comes as a result of respiratory paralysis. 

Treatment 

There is no treatment or antidote, since curare 
works so quickly. 



80 q'anide 



cyanide [Other names: hydrogen cyanide (prussic 
acid), potassium cyanide, sodium cyanide.] The 

various forms of cyanide (gas, salts) can be swal- 
lowed, inhaled, or absorbed through the skin, and 
it is one of the most rapidly acting poisons known. 
The inhalation of cyanide in its extremely volatile 
form called hydrocyanic acid (or prussic acid) can 
be fatal in just a few minutes. Hydrocyanic acid 
occurs naturally in a large variety of seeds and pits 
(such as peach, apricot, apple, plum, etc.) and has 
many industrial uses. 

In addition, many other plants have cyanogenic 
glycosides that have a similar effect, although they 
take longer to act. These amygdalin-containing 
fruit seeds include choke cherries, cassava beans, 
and bitter almonds. 

Hydrogen cyanide is found in fumigants, insec- 
ticides, rat poisons, metal polish, and electroplating 
solution and has also been used in gas chambers. 
Potassium cyanide and sodium cyanide are both 
white solids smelling faintly of bitter almonds. 
Certain cyanides irritate the eyes so powerfully 
that they have been used in some types of tear gas. 
In the household, cyanide can be found in many 
products from silver polish to rat poison. 

Symptoms 

Cyanide prevents the body's red blood cells from 
absorbing oxygen by interfering with the body's 
enzymes. When the cells can't get oxygen, they 
produce a rapid progression of symptoms; a person 
who swallows or smells too much cyanide can lose 
consciousness, fall into convulsions, and die within 
1 5 minutes. Mortality from cyanide may be as high 
as 95 percent. 

Treatment 

Call poison control before attempting any treat- 
ment, which must be rapid. Do not induce emesis. 
An antidote kit (containing amyl nitrite perles and 
intravenous sodium nitrite and sodium thiosulfate) 
is available. The longer the patient can be kept 
alive the better the prognosis, since the body can 
neutralize cyanide by combining it with sulfur 
compounds to form inactive sulfocyanates. A new 
fast-acting antidote (within three minutes) was 
discovered by researchers at the University of Min- 
nesota Center for Drug Design and Minneapolis 



VA Medical Center in 2007 and was slated to enter 
human clinical trials within three years. 

See also cherries, wild and cultivated; cyano- 
genic glycosides; Prunus. 

cyanogenic glycosides A toxic glycoside (a com- 
pound found in plants that contains sugar) that 
gives off hydrocyanic acid and other cyanide com- 
pounds when exposed to acids and enzymes in 
the digestive tract. When this hydrogen cyanide 
is produced by cyanogenic glycosides, it interferes 
with the level of oxygen in the blood and causes 
the blue skin coloring common in cyanide poison- 
ing. Cyanogenic glycosides are found in apricot, 
cherry, and peach pits, and apple seeds, but they 
are released only if the pits of seeds are ground 
and eaten; if swallowed whole, they cause no harm 
because of the hard outer shell covering. 

See also cherries, wild and cultivated; cyanide; 
Prunus. 



cyclohexane hexachloride See lindane. 

cyclopropane A flammable general anesthetic 
not widely used today because of its high cost and 
explosive nature. Cyclopropane works by depress- 
ing all functions of the central nervous system. 

Symptoms 

When given in large amounts, this anesthetic will 
stop breathing with possible damage to heart, liver, 
and kidneys. Symptoms include stupor, uncon- 
sciousness, and respiratory paralysis. Convulsions 
may follow. 

Treatment 

Symptoms will disappear once the anesthetic is 
removed. Keep warm, provide CPR if required. 
Stabihze blood pressure. 

See also anesthetic, gaseous/volatile. 

Cyclospora A one-celled organism, Cyclospora 
causes symptoms similar to Cryptosporidium and 
led to illness in hundreds of residents of at least 



Cyclospora 81 



a dozen states in a 1995 outbreak. Like Cryptospo- 
ridium, Cyclospora pollutes water and taints food. 
The infection (cyclosporiasis) is spread from the 
fecal-oral route, both from person to person and 
via tainted water or food. 

The United States has battled several cyclospora 
epidemics which began in the spring of 1996 and 
one included an outbreak in the 1 1 states east of 
the Rocky Mountains that caused 1,000 people to 
get sick from contaminated raspberries. Another 
raspberry-related outbreak affected 54 people at a 
wedding reception in Philadelphia in 2000. Since 
the infection is fairly new, experts believe many 
cases are simply not diagnosed or reported. Doctors 
must specifically request testing for Cyclospora; it is 
not detected by routine lab tests. 

Some cases have been traced to contaminated 
strawberries, others to raspberries or mixed fruit. 
In other cases, experts can't find the original source 
of the infection. 

Symptoms 

One to two weeks after infection, symptoms of 
diarrhea, nausea and vomiting appear, together 
with fever and stomach pain. Symptoms may be 
intermittent over the course of the disease, which 
can last for several weeks. While rarely fatal. 



untreated diarrhea can cause severe dehydration, 
which can be a serious health threat to very young 
children, very old people, and people with faulty 
immune systems. If not treated, symptoms may last 
for a few days to a month or more. 

Diagnosis 

Special lab tests can identify the parasite in stool, 
which may require specimens collected over sev- 
eral days. 

Treatment 

A combination of two antibiotics, trimethoprim 
and sulfamethoxazole, can control the infection; 
otherwise, rest and plenty of fluids. 

Prevention 

Wash hands often, especially if you change dia- 
pers or work around young children. Thoroughly 
wash fruits and vegetables before eating. Infected 
people should not prepare food that is eaten raw. 
Certain areas of high infection should boil water 
for one minute before use. The organism doesn't 
appear to be killed by iodine or chlorine and can 
even elude filtration systems. The only thing that 
kills this parasite is boiling the water in which it 
lives. 



D 



daffodil (Narcissus) [Other names: jonquil, white 
narcissi] The creamy or yellow flowers of the 
daffodil can be seen throughout temperate North 
America. This spring-flowering bulb has been 
recorded in history as early as the second century 
B.C. and is extremely popular today in gardens. 
Daffodils have a trumpet-shaped center against 
star-shaped petals, with the trumpet often being 
a contrasting color. The plant stands around 2 
feet tall with five-inch blooms. There are about 
50 species of daffodil and more than 13,000 
hybrids. 

Poisonous part 

The leaves, berries, stems, and roots all contain 
toxic compounds, but the most potent concentra- 
tion is found in bulbs, also referred to as rhizomes 
or corms. The flowers are not toxic. Poisonous 
substances are alkaloids, including masonin and 
homolycorine. Most poisonings occur in children 
who eat the leaves, bulbs, or stems. During World 
War II, starving cattle in the Netherlands were fed 
daffodil bulbs when feed suppfies dwindled, and 
the animals were fatally poisoned. Bulbs should 
be kept in a secure place away from food areas, 
where they may be mistaken for onions, and 
clearly marked. 

Symptoms 

Alkaloids may cause dizziness, abdominal pain, 
diarrhea, and nausea. Convulsions and death may 
occur if enough of the plant has been consumed. 
Some people who handle daffodils commercially, 
especially florists and flower growers, frequently 
experience daffodil dermatitis ("daffodil itch"), 
which occurs when they make contact with the 
sap of the bulbs and stems. 



Treatment 

Induce vomiting and administer copious amounts 
of fluids; introduce activated charcoal and treat 
symptoms. 



Dalmane (flurazepam) An anticonvulsant and a 
muscle relaxant used to relieve anxiety, Dalmane is 
not as strong as Vafium (diazepam) but is still con- 
sidered toxic. This is a drug often chosen for suicide 
when combined with alcohol. It reacts negatively 
with other anticonvulsants, antidepressants, anti- 
histamines, antihypertensives, oral contraceptives, 
disulfiram, erythromycins, monoamine oxidase 
(MAO) inhibitors, narcotics, sedatives, sleeping 
pills, and tranquilizers. 

Symptoms 

Within 10 to 20 minutes of ingestion, patients 
become groggy and fall into sleep, dropping fur- 
ther into unconsciousness if a large dose has been 
taken. Withdrawal psychosis is also possible. 

Treatment 

Gastric lavage; increase oxygen while maintaining 
blood pressure. 
See also diazepam. 



dantrolene This drug is used in the treatment 
of the very high fevers common in anesthesia 
overdose. It is not, however, a substitute for other 
means of controlling temperature such as sponging 
and fanning. Dantrolene is a muscle relaxant that 
may cause diarrhea, muscle weakness, and, some- 
times kidney damage. 



82 



DDT 83 



daphne (Daphne) [Other names: bois joli, copse 
laurel, dwarf bay, February daphne, flax olive, lady 
laurel, spurge flax, spurge laurel, spurge olive, wild 
pepper, winter daphne, wood laurel.] One of the 

oldest plants recognized as a poison, daphne is 
found throughout the British Isles, the northeast- 
ern United States, and eastern Canada. It is widely 
planted as an ornamental and is sometimes kept 
indoors as a flowering houseplant. This unusually 
fragrant rounded shrub has clusters of purple or 
white flowers that grow in the spring before the 
leathery leaves appear. Fruits are scarlet or yellow 
with a pit. Of all the daphne species, the Daphne 
mezereum variety is the most deadly, although all 
species are considered poisonous. 

Poisonous part 

All parts of this plant are poisonous, especially 
the berries, bark, and seeds; berries of D. mezereum 
are bright red; those of D. laureola are green, then 
blue and finally black when fully ripe. Poison- 
ous substances are the glycoside daphnetoxin and 
mezerein, an irritating, bhstering resin. This plant is 
considered particularly dangerous to children. 

Symptoms 

Symptoms appear in 45 minutes to several hours 
and include swelling and blistering of the lips, 
salivation and problems in swallowing, burning 
and ulceration in the digestive tract, stomach pain, 
vomiting, bloody diarrhea, weakness, convulsions, 
shock, coma, and death. Just a few berries can be 
fatal to a child. This plant may also cause systemic 
damage to the kidneys. 

Treatment 

Gastric lavage with caution, since the mucous 
membranes may have been damaged as a result of 
this poison. Victims often go into shock after poi- 
soning with daphne. 

Darvon See narcotics. 

datura See jimsonweed. 

DDT (dichlorodiphenyltrichloroethane) One of 

a group of chlorinated hydrocarbons, this insect- 



fighting chemical was once widely used in agri- 
culture and malarial control programs around the 
world. It was developed in Switzerland in the early 
1940s and was found to be much more effective 
than previous insecticides and became an impor- 
tant weapon in fighting insect-transmitted diseases. 
Unfortunately, some insects have adapted to the 
poison and are resistant to its effects. However, 
because of its toxicity, it was banned in the United 
States in 1973 because it does not disperse in the 
environment but accumulates in biological systems. 
It is still used in some other parts of the world. 

This broad-spectrum insecticide dissolves easily 
in oil and therefore builds up in fatty tissue; eating 
animals that have consumed DDT — or even that 
have eaten others that have consumed DDT — will 
poison anyone who eats the meat. 

While it can be inhaled or absorbed through the 
skin, the most common means of human exposure 
is by eating DDT-contaminated food. In fact, inhal- 
ing the dust or coming in contact with the solution is 
rarely harmful to humans unless the person is wear- 
ing some sort of oily insect repellent that would aid 
absorption. However, toxic doses are possible if the 
skin contact area is large or the exposure lengthy. 

Symptoms 

DDT affects the central nervous system, causing 
muscle weakness, excitability and convulsions, 
with tremor, confusion, headache, numbness of 
the tongue, lips and face, and vomiting. Twitchings 
begin in the face and proceed in rising strength to 
involve all muscles. In fact, attacks resemble the 
convulsions of strychnine poisoning, since they can 
be set off by light or noise. Respiratory arrest and 
heart attack are followed by death. 

Chronic poisoning causes weight loss, headache, 
loss of appetite, nausea, eye irritation, weakness, 
and increasing tremors followed by convulsions, 
coma, and death. 

Contact with the eyes may cause temporary 
bhndness. People who work with DDT may also 
experience a gradual sensitization and allergic reac- 
tions to the chemical. 

Treatment 

If convulsions continue for some time, recovery 
is not likely. Treat symptoms, and perform gastric 



84 deadly cort 



lavage, but do not induce vomiting. Administer 
activated charcoal and a cathartic. Stimulants (such 
as epinephrine) may induce heart attack; admin- 
ister anticonvulsants (such as Valium) to control 
convulsions. 

See also chlorinated hydrocarbon pesticides. 



deadly cort See galerina mushrooms. 

death camas (Zigadenus venenosus) [Other names: 
alkali grass, black snake root, hog's potato, mystery 
grass, poison sego, sand corn, soap plant, squirrel 
food, water lily, wild onion.] One of the lily family 
and often mistaken for an onion, the death camas 
is found throughout North America (especially the 
extreme southeast) and Alaska and Canada. 

Leaves are grassy and long and narrow — up 
to two feet tall — and at the top, the stem has a 
branched cluster of greeny white to yellow flowers. 
The plant's bulb looks like an onion, but does not 
have an oniony odor. 

Poisonous part 

Fresh leaves, stems, bulbs, and flowers are poison- 
ous, but the seeds are particularly deadly. Poisons 
include zygacine, veratrine and zygadenine, pro- 
toveratridine, iso- and neogermidine. While cattle 
are usually poisoned by death camas, it is possible 
for humans to be poisoned as well. 

Symptoms 

Symptoms appear within one hour and include 
burning of the mouth, vomiting, thirst, weakness, 
slow heartbeat, staggering, paralysis, convulsions, 
coma, and death. 

Treatment 

There is no antidote, but gastric lavage should be 
performed if the victim has not vomited. Fluids and 
the administration of atropine or ephedrine may 
also be required. 

death cap/death cup (Amanita plialloides) One 

of the deadliest members of the Amanita genus of 
mushrooms, the death cap or death cup is found in 



woods or their borders and is responsible for most of 
the fatalities associated with mushroom poisoning. 
It has a green or brown cap and appears in summer 
or early fall. Some experts also include the destroy- 
ing angel as part of the Amanita phailoides group. 

Poisonous part 

This deadly mushroom contains peptide toxins, 
phalloidin and two amanitins that damage cells 
throughout the body within six to 12 hours after 
ingestion. The toxins are not affected by drying, 
cooking, or boiling in water. 

Symptoms 

First symptoms are caused by the action of the 
amatoxins on the intestine, but this is not respon- 
sible for the ultimate outcome. Twelve hours after 
ingestion, symptoms include violent abdominal 
pain, vomiting, bloody diarrhea, loss of fluid, and 
intense thirst. A latency period follows, up to five 
days, but by then the toxins have damaged the 
liver, kidneys, and central nervous system. There 
is a decrease in urinary output and a drop in sugar 
levels in the blood, which leads to coma and — more 
than 50 percent of the time — death. 

Treatment 

During the first phase, give fluids and monitor 
electrolytes; urine flow should be maintained, and 
repeat doses of activated charcoal may be given. If 
management is successful, the victim will recover 
within one week. Various strategies have been 
tried to treat this type of mushroom poisoning 
in Europe, including massive doses of vitamins, 
corticosteroids, sex hormones, high-dose glucose, 
penicillin G, and thioctic acid. None of these has 
been proven effective. 

See also Amanita mushrooms; mushroom 
poisoning. 



decongestants A range of drugs used to reheve 
nasal congestion, they work by constricting blood 
vessels in the nose, which reduces swelling. They 
are used to treat sinusitis, allergies, and acute upper 
respiratory infections. 

Decongestants include phenylpropanolamine 
(PPA), phenylephrine (PHE), ephedrine (EPH), and 



derris 85 



pseudoephedrine (PEP); all but PPA are available 
over the counter as nasal decongestants and cold 
preparations that usually contain antihistamines 
and cough suppressants as well. Combinations of 
these drugs with caffeine are sold on the street as 
amphetamine or cocaine substitutes. 

iVIany of these drugs react negatively with other 
drugs. Patients sensitive to epinephrine, ephedrine, 
terbutahne, or amphetamines may also be sensitive 
to drugs such as PPA. 

In November 2000, the Food and Drug Admin- 
istration (FDA) issued a public health warning to 
consumers, advising them to stop using any medi- 
cations that contained PPA, as research showed 
there was a risk of hemorrhagic stroke associated 
with its use. The FDA also asked drug manufactur- 
ers to discontinue the marketing and sales of over- 
the-counter medications that contained PPA, and 
stores across the United States pulled these drugs 
from their shelves. 

Symptoms 

Poisoning with products containing PPA, PHE, and 
EPH may provoke symptoms after ingesting just 
two or three times the recommended dose. PEP is 
slightly less toxic (symptoms occur with four to five 
times recommended dose). 

Patients taking monoamine oxidase (MAO) 
inhibitors may be extremely sensitive to these 
drugs, developing severe high blood pressure after 
ingesting even less-than-recommended doses. 

The most serious symptom of these drugs is 
severe high blood pressure, together with hyper- 
tensive complications of headache, confusion, 
seizures, and stroke. In fact, intracranial hemor- 
rhage may occur in even normal, healthy young 
people after only a slight rise in blood pressure. 
The high blood pressure caused by PPA and PHE 
occurs together with slow heartbeat, while EPH 
and PEP usually cause high blood pressure with 
rapid heartbeat. 

Using antihistamines or caffeine may increase 
the high blood pressure with PPA and PHE. PPA 
may also cause heart attack and stroke. 

Treatment 

There is no specific antidote. Give symptomatic 
treatment; monitor vital signs and electrocardio- 



gram. Do not use beta blockers to treat high blood 
pressure without first giving a vasodilator (phen- 
tolamine or nitroprusside), for they will worsen 
the high blood pressure. Do not induce vomiting 
because of the danger of worsening the high blood 
pressure. Perform gastric lavage if the victim has 
ingested the drug within 30 to 60 minutes or has 
taken a large dose. Administer activated charcoal 
and a cathartic. 



deferoxamine This specific chelating agent is 
used in the treatment of iron overdose, particu- 
larly in the presence of shock, acidosis, severe gas- 
troenteritis, leukocytosis, and high blood sugar. 
It binds to the circulating free iron, and both are 
excreted in the urine, turning it an orange-pink 
color. Deferoxamine is also sometimes used to 
determine the presence of free iron in the body 
by administering the chelating agent and then 
looking for the characteristic pinkish rose color of 
the urine. 

See also iron in drugs and supplements. 



Demerol See meperidine; narcotics. 
Depakene See valproic acid. 
derrin See rotenone. 



derris The powdered root of various species of 
the botanical genus Derris, used as an insecticide. It 
is also used to kill fish without damaging the food 
supply, enabhng game fish to be introduced into 
the same body of water. The toxic principles of der- 
ris include rotenone. 

Symptoms 

When absorbed through the skin, derris root may 
cause dermatitis. It is also more toxic than its rote- 
none and rotenoid content would suggest; it is 
believed this discrepancy may be due to the pres- 
ence of other toxic agents in the derris powder. 
Absorption and toxicity are enhanced by olive oil. 



86 destroying angel 



Treatment 

Symptomatic and supportive, including removal 
of the material from the skin and gastrointestinal 
tract. Oily cathartics should not be used, since 
absorption may be increased by their use. 
See also rotenone. 



destroying angel (Amanita bispongera [smaller 
death angel], A. ocreata, A. verna [fool's angel] and 
A. virosa [destroying angel or death angel]) A 

mushroom of the poisonous Amanita genus, the 
destroying angel (and its close relatives, named 
above) are extremely deadly, with a 90 percent 
fatality rate and no known antidote. 

The fool's angel is the most common; it is 
relatively smaller than the others and chalky 
white. The destroying angels have a large white 
body and are found in forests during wet periods 
in summer and autumn. Experts disagree as to 
the classification of these related mushrooms, 
which is why they are listed together here. These 
amanitas are found in the mid-Atlantic states to 
Florida and west to Texas and are found in dry 
pine woods, although the smaller death angel can 
also be found in wooded lawns, especially near 
oak trees. 

Poisonous part 

The main poisons found in these mushrooms are 
the slow-acting amanitin and the fast-acting phal- 
loidin. Amanitin causes most of the symptoms, and 
phalloidin causes degeneration in kidney, liver, and 
heart muscles. These mushrooms are deadly; one 
or two cooked mushrooms can be fatal, and there 
exists a report that one-third of one raw cap has 
killed a child. 

Symptoms 

After these mushrooms are eaten, there are typically 
no symptoms for six to 1 5 hours — and sometimes 
as long as two days. Symptoms begin suddenly with 
severe abdominal pain, nausea, vomiting, and diar- 
rhea, followed by extreme abdominal pain, exces- 
sive thirst, violent vomiting, urinary problems, 
weakness, jaundice, convulsions, coma, and death. 
Severe dehydration eventually results in cardiac 
arrest. Death occurs within two days of ingestion of 



a large amount of mushrooms, but more generally 
it may take up to three days of remissions followed 
by repeated, more acute attacks. Death occurs in 
50 to 90 percent of cases. Recovery can take up to 
one month. 

Treatment 

There is no known antidote, although some victims 
survive if given a liver transplant. Gastric lavage is 
also instituted. Animal studies suggest that early 
treatment with penicillin G, silibinin, or cimetidine 
may partially protect against liver injury. Treat fluid 
and electrolyte loss to head off massive circulatory 
collapse. 

See also Amanita mushrooms; mushroom 

POISONING. 



dextromethorphan Found in many over-the- 
counter cough and cold medicines, dextrometho- 
rphan is frequently involved in poisonings with 
children, although fatalities are rare. Dextrometho- 
rphan is also frequently combined with antihista- 
mines, decongestants, or acetaminophen. It is a 
popular choice for cough suppressants because it 
works as well as codeine but is not addictive. 

Symptoms 

Toxicity depends on other ingredients in the par- 
ticular product that was ingested. Mild overdoses 
cause ataxia, clumsiness, restlessness, and some- 
times visual and auditory hallucinations. More seri- 
ous overdoses produce stupor, coma, and breathing 
problems, especially if alcohol has been ingested at 
the same time. In addition, persons taking mono- 
amine oxidase inhibitors who ingest a normal dose 
of dextromethorphan may experience high blood 
pressure and very high fever. 

Treatment 

Mild overdoses require only supervision; in 
more severe cases, the drug naloxone has reported 
to be an effective antidote in some cases, but not in 
others. Induce vomiting or perform gastric lavage; 
administer activated charcoal and a cathartic. 



DFP See narcotics. 



dieldrin 87 



diarrheic shellfish poisoning Although this type 
of diarrhea-causing shellfish poison has not been 
confirmed in the United States, the organisms that 
produce the poison are found in U.S. waters and 
an outbreak has been confirmed in eastern Canada. 
DSP is associated primarily with mussels, oysters, 
and scallops. 

Symptoms 

This type of shellfish poisoning begins within 30 
minutes to two or three hours, depending on the 
amount of tainted shellfish eaten. Symptoms (nau- 
sea, vomiting, diarrhea) may last as long as two or 
three days, but recovery is complete with, no afteref- 
fects and the disease is not usually life threatening. 

Treatment 

No treatment is necessary. 

diazepam (Valium) One of the group of ben- 
zodiazepines used in the treatment of anxiety or 
agitation caused by hallucinogenic drug overdose; 
to control seizures because of convulsant drug 
overdose; and to relax excessive muscle rigidity 
and contractions following strychnine poisoning or 
the bite of the black widow spider. 

See also benzodiazepines; black widow spider; 

STRYCHNINE. 



dieffenbachia (Dieffenbachia) [Other names: 
dumb cane, dumb plant, mother-in-law's tongue, 
tuft root.] This extremely common plant has 
been used indoors as an attractive fohage house- 
plant for hundreds of years, but it can cause mouth 
pain if ingested and can be fatal in large amounts. 

There are a number of dieffenbachia species, 
including D. amoena, D. bausei, D. Candida, D. exotica, 
D. maculate, and D. seguine. Dieffenbachia belongs 
to the family Araceae, which also includes other 
ornamental plants such as the jack-in-the-pulpit, 
philodendron, pothos, and calla lily. 

These shade-loving plants have bright green 
oblong leaves and can grow quite tall, with fleshy 
stems as much as an inch thick. They may be 
found in outdoor gardens in southern Florida and 
Hawaii. 



Dieffenbachia's toxic qualities have been known 
for a long time; in the past, slaves were punished 
by rubbing their mouths with dieffenbachia, and 
there are reports that the Nazis experimented with 
this plant in concentration camps during World 
War II. 

Poisonous part 

All parts of this plant (including the sap) contain 
potent irritants including proteolytic enzymes, 
raphides of calcium oxalate, and other, unknown 
toxins. The calcium oxalate raphides in this plant 
are really sharp crystals that puncture tissue; it is 
possible that the plant contains enzymes that attack 
cells through the punctures. The mechanisms 
behind its ability to cause systemic poisoning as 
well as localized irritation are not known. 

Symptoms 

All varieties of dieffenbachia contain a range of 
potent irritants that can cause serious tissue dam- 
age to eyes, skin, and mucous membranes. Chew- 
ing a leaf from this plant causes almost immediate, 
intense pain, blistering and burning of the mouth 
and tongue, excess salivation, swelling of the tongue 
and throat, and difficulty in swallowing. Pain and 
swelling may persist for several days and leave dam- 
aged tissue behind. Because of the immediate pain 
upon ingestion, poisoning with large amounts of the 
plant is unlikely; however, in this event the toxins 
can swell the throat tissue, blocking the airway and 
leading to death. Some sources report that dumb 
cane can also cause systemic poisoning resulting 
in nausea, vomiting, and diarrhea and damage to 
internal organs. The name "dumb cane" comes from 
its tendency to paralyze vocal cords. 

Treatment 

Pain and swelling in the mouth will slowly fade 
even without treatment, although cool liquids 
(such as milk or Popsicles) and painkillers may 
help. Perform gastric lavage, and give antihista- 
mines for local swelling. 
See also philodendron. 



dieldrin [Trade names: Compound 497, HEOD, 
Octalox.] A highly toxic chlorinated hydrocarbon 



88 digitalis 



pesticide used against potato beetles, corn pests, 
and rape plant parasites. Its manufacture in the 
United States was banned in 1974 under the Envi- 
ronmental Protection Agency (EPA) Fungicide and 
Rodenticide Act, although it is still produced for 
use in Holland. 

Dieldrin is highly soluble in fat, where it accu- 
mulates in humans or animals until a toxic level is 
reached. It can be inhaled, absorbed, or ingested 
and is particularly dangerous when heated, as it 
can give off very toxic chloride fumes. 

Symptoms 

Within 20 minutes to 12 hours dieldrin produces 
headache, dizziness, nausea, vomiting, sweating, 
excitability, irritability, convulsions, coma, and 
death. 

Treatment 

There is no specific antidote. Perform gastric lavage 
but do not induce vomiting because of the risk 
of sudden onset of seizures; administer activated 
charcoal and a cathartic. Irregular heartbeat may 
respond to propranolol. 

See also chlorinated hydrocarbon pesticides. 



digitalis A group of drugs used as a heart medi- 
cine that are purified from the seeds and leaves 
of the common foxglove plant (Digitalis purpurea). 
Digitalis strengthens and slows contractions of 
the heart and restores circulation in persons with 
congestive heart failure. It also slows the rate of 
ventricular contraction in those with atrial fibril- 
lation. In small doses, digitalis can strengthen a 
weak heart and slow down a rapid heartbeat; in 
large doses, however, it can be fatal by danger- 
ously slowing down heart function. The most 
commonly used drugs in this group are digoxin 
and digitoxin. 

The active principles in digitalis include a group 
of steroids called cardiac glycosides. Dosage must 
be measured with extreme care, since the lethal 
dose is only three times the effective dose. 

Symptoms 

Overdose is evident with both gastrointestinal and 
neurologic problems, including anorexia, nausea. 



vomiting, diarrhea, depression, visual disturbances, 
fatigue, headache, dehrium, confusion, and hal- 
lucinations. A wide variety of cardiac problems are 
common and represent the most serious form of 
toxicity. 

Treatment 

Management of mild overdose may require only 
stopping the drug. Acute poisoning requires gas- 
tric lavage or induced vomiting, followed by the 
administration of activated charcoal and a cathartic 
as soon as possible after ingestion. 

See also cardiac glycosides; digitoxin; digoxin; 

FOXGLOVE. 



digitoxin This cardiac glycoside is used to regu- 
late the heart's rhythm after a congestive heart 
failure, increasing contractions and reducing fluid 
retention. While some physicians have prescribed 
digitoxin to treat obesity, its adverse affects can be 
fatal. 

Symptoms 

Almost immediately, overdose causes nausea, vom- 
iting, diarrhea, blurred vision, and heart problems 
such as premature contractions and heart rhythm 
disturbances. 

Treatment 

Wash the stomach with tannic acid (strong tea) 
and keep the victim lying down. Give stimulants 
such as caffeine, ammonia, or atropine; if the 
pulse drops below 50 beats per minute, atropine is 
administered. 

See also digitalis; digoxin; foxglove. 

digoxin (Lanoxin) This cardiac glycoside is used 
to regulate the heart's rhythm after a congestive 
heart failure, increasing contractions and reducing 
fluid retention. 

Symptoms 

Within six hours, overdose causes nausea, vom- 
iting, diarrhea, blurred vision, and heart prob- 
lems such as premature contractions and atrial 
fibrillation. 



dinoflagellate 89 



Treatment 

Discontinue administration; acute ingestion 
requires induced vomiting, gastric lavage, and the 
administration of activated charcoal and a cathartic 
as soon as possible. 

See also cardiac glycosides; digitalis; digitoxin. 

digoxin-specific antibodies The antidote for poi- 
soning by digoxin and, to some degree, digitoxin 
and other cardiac glycosides. Digoxin-specific anti- 
bodies are produced in immunized sheep and 
can reverse the signs of digitalis poisoning within 
30-60 minutes of administration with complete 
reversal within three hours. 

See also cardiac glycosides; digitoxin; digoxin. 

Dilantin See phenytoin. 



Dilaudid See hydromorphone. 



dimercaprol This chelating agent is used to treat 
poisoning of arsenic, mercury, lead, antimony, bis- 
muth, chromium, copper, nickel, tungsten, zinc, or 
gold. It is not effective in the treatment of iron, sele- 
nium or cadmium poisoning. Dimercaprol is toxic; 
about 50 percent of patients taking six milligrams 
per kilogram intramuscularly (2.5 mg/kg is normal) 
develop reactions such as hypertension, nausea, 
vomiting, chest pain, headache, and tachycardia. 

dimethyl sulfate (sulfuric acid dimethyl ester, 
methyl sulfate) This colorless, odorless oily liquid 
is used to manufacture dyes, drugs, pesticides, and 
perfumes; most poisonings occur when liquid or 
vapors leak from industrial machines. Its very mild 
oniony odor is barely perceptible and not useful as a 
warning. Dimethyl sulfate does not dissolve readily 
in water but does dissolve well in organic solvents. 

Symptoms 

When absorbed through the skin or eyes, it is 
extremely irritating, although there is a latency 
period of up to five hours. Exposure to the vapors 



produces an immediate reaction of runny eyes and 
nose and swelling of the mouth, lips, and throat, 
with hoarseness and sore throat. There may also be 
conjunctivitis (pink eye), perforation of the nasal 
septum similar to the side effects of cocaine, and 
permanent vision problems. Liver and kidneys may 
also be damaged. 

Upon ingestion, dimethyl sulfate hydrolyzes 
to sulfuric acid and methanol. Ingestion causes 
breathing problems and bronchitis within 1 2 hours, 
together with central nervous system side effects 
including drowsiness, temporary bhndness, heart 
irregularities, and irritation, followed by convul- 
sions and death from pulmonary edema. Dimethyl 
sulfate causes cancer in animals. 

Treatment 

Symptomatic treatment, including hydrocortisone 
to reduce injury. 

dinoflagellate (Gonyaulax catenella, G. tamarensis 
and others) The organisms responsible for "red 
tide," dinoflagellates are extremely toxic one- 
celled aquatic animals found on the Pacific coast 
of North America (G. catenella) and the east coast 
of North America (G. tamarensis). Dinoflagellates, 
some of which (Noctiluca) also produce part of the 
luminescence in the sea, have the characteristics 
of both plants and animals; most are microscopic 
and marine. A person becomes poisoned with 
dinoflagellates when eating contaminated shellfish; 
primarily, dinoflagellates cause paralytic shellfish 
poisoning, although at least one variety causes a 
type of poisoning more similar to ciguatera. 

Under good conditions (warm climate, warm 
water), dinoflagellates may reach 60 million organ- 
isms per liter of water; these rapid growths (referred 
to as a "bloom") cause red tides that discolor the sea 
and poison fish and marine life. Usually, a person 
becomes poisoned with dinoflagellates when eating 
shellfish that have been feeding on the toxic proto- 
zoa. Bivalve shellfish (mussels, clams, and oysters) 
are the primary shellfish at risk, and mussels are 
the most susceptible. Healthy bivalve shellfish filter 
large amounts of dinoflagellates, which form the 
primary ocean food from May through August. 
During these warm times, the dinoflagellates thrive 



90 dioxins 



by photosynthesis and can be so invasive that they 
kill birds and fish. 

The first large epidemic of poisoning caused 
by dinoflagellate-contaminated shellfish occurred 
in San Francisco in 1927, when 102 people were 
sickened and six died. Today, largely because of the 
prohibition against eating certain shellfish during 
the summer months, such epidemics are rare. 

Still, red tides and the resultant paralytic shellfish 
poisoning (PSP) and ciguatera are a problem in the 
warm months (May to November) on the Pacific 
coast between central California and the Aleutian 
Islands and on the Atlantic coast (St. Lawrence 
River estuary in Canada, the Bay of Fundy, and 
several northeastern states in the United States). 
Other countries have also experienced outbreaks 
of PSP, including England, Wales, France, Scotland, 
Germany, Norway, Ireland, Belgium, Denmark, 
Portugal, South Africa, Japan, New Guinea, and 
New Zealand. 

Not all dinoflagellate species are toxic to humans 
or marine creatures, and many varieties of phy- 
toplankton bloom to large proportions without 
causing harm. Harmful dinoflagellates found in 
North America include G. catenella, G. acatenella, 
and G. tamarensis, all of which cause PSP; G. breve, 
found on the Florida Gulf coast, which causes a 
ciguatera-like poisoning; and G. polyedra, found on 
the southern California coast, causing a paralytic 
poison different from PSP. In Japan, the dinoflagel- 
late Exuviaella mariaelehouriae causes "oyster poi- 
soning," damaging the liver and kidneys. Several 
other dinoflagellates are injurious to fish and other 
marine creatures but do no harm to humans. 

Symptoms 

Similar to curare poisoning and extremely fast 
acting (within 10 minutes), dinoflagellate poison- 
ing causes a tingling and burning sensation and 
numbness of the lips, tongue, and face, spreading 
elsewhere to the body; it can also cause weakness, 
dizziness, joint pain, intense thirst, and difficulty 
in swallowing. As the illness progresses, breath- 
ing problems and muscular paralysis become more 
severe. Death is caused by respiratory paralysis 
within two to 12 hours, depending on the dose. 
Fatalities occur in 10 percent of poisoning cases. 
If the victim survives for 24 hours, prognosis is 



good and there do not seem to be lasting effects of 
poisoning. 

Treatment 

There is no antidote for shellfish poisoning caused 
by dinoflagellates. Gastric lavage and activated 
charcoal may be administered, since saxitoxin is 
readily absorbed by charcoal. It may be neces- 
sary to monitor blood pressure and the heart, and 
to provide respiratory support, since patients are 
often in critical condition. 

See also ciguatera; paralytic shellfish poison- 
ing; SHELLFISH POISONING. 

dioxins A group of highly toxic substances used 
in a variety of industrial and other applications. 
The herbicide Agent Orange used during combat in 
Vietnam contained small quantities of one type of 
dioxin. However, diagnosis of dioxin poisoning is 
difficult, since it is hard to detect dioxin in blood or 
tissue and there is no estabhshed correlation with 
symptoms. 

According to research released by the Environ- 
mental Protection Agency, dioxin is a potent carcin- 
ogen with subtle immunological, developmental, 
and neurological effects that may be even more of a 
public health threat than its carcinogenic problems. 
A July 2002 study found dioxins to be significantly 
related to an increase in breast cancer. 

Dioxin has spread well beyond its main indus- 
trial sources (paper processors, herbicide manufac- 
turers, and garbage incinerators) and can be found 
today in the bodies of anyone who eats fish, meat, 
or dairy products. Research suggests dioxin may 
affect the body's hormonal messenger system; it 
may affect sex hormones and insulin and could 
create permanent health problems for children 
exposed in the womb — lowering sperm counts, 
interfering with sexual development, and impair- 
ing brain development. 

Symptoms 

After exposure, victims experience skin, eye, and 
mucous membrane irritation, nausea, and vomit- 
ing. After a latency period of up to several weeks, 
additional symptoms appear, including chloracne, 
excessive hair growth, pigment abnormafities. 



diuretics 91 



motor weakness, and sensory impairments. In ani- 
mals, death occurs a few weeks after a letlial dose 
as ttie result of a wasting syndrome in which the 
animal stops eating and loses weight. 

Treatment 

There is no specific antidote, only symptomatic 
treatment, with induced vomiting or gastric lavage 
followed by the administration of activated char- 
coal and a cathartic. For eye or skin contamina- 
tion, flush with water and soap; irrigate eyes with 
tepid water or saline. Anyone helping to wash the 
affected clothing or skin should wear protective 
clothing. 

diphenhydramine This antihistamine is used both 
as a treatment for the itchy skin rash from a wide 
variety of plants (such as poison ivy or sumac) and 
to partially prevent anaphylaxis caused by horse 
serum-based antivenins or antitoxins. 
See also antivenin. 



diphyllobothriasis A type of food poisoning caused 
by eating fish infested with a broad fish tapeworm 
(Diphyllobothrium latum). Now uncommon in the 
United States, it was formerly often found in the 
Great Lakes area, where it was known as "Jewish, 
or Scandinavian, housewife's disease" because the 
preparers of gefilte fish or fish balls tended to taste 
their food as they prepared it, before fish was fully 
cooked. The parasite is now supposedly absent from 
Great Lakes fish; recently, however, cases have 
been reported along the west coast. 

Foods are not routinely analyzed for this para- 
site. In 1980, an outbreak involving four Los 
Angeles physicians occurred when they all ate 
sushi made of tuna, red snapper, and salmon. At 
the time of this outbreak, there was also a general 
increase in requests for niclosamide (the drug used 
to treat the infestation). Interviews of 39 patients 
with similar symptoms at the time showed that 32 
remembered eating salmon before becoming sick. 

The disease is caused by parasitic flatworms and 
other members of this tapeworm family; the larva 
are often found in the viscera of fresh and marine 
fishes. After eating an infected fish, an adult tape- 



worm between 3 and 10 feet long grows in the 
small intestine; about a month later, it releases 
more than a milhon eggs into the stool every day. 
Infection is usually limited to one worm. 

It is found in freshwater fish, or fish that migrate 
from salt water to freshwater for breeding, includ- 
ing pike, salmon, trout, whitefish, and turbot. 

Symptoms 

Symptoms appear about 10 days after eating raw 
or poorly cooked fish. Many people don't have any 
symptoms, but others report a variety of minor 
complaints including distended abdomen, flatu- 
lence, nausea, headache, nervousness, weakness, 
cramping, and diarrhea. Some report a sensation 
that "something is moving inside." Those who are 
susceptible (usually those of Scandinavian heri- 
tage) may experience a severe anemia as a result of 
this tapeworm infection, caused by the tapeworm's 
absorption of vitamin B12. 

Diagnosis 

The disease is identified by finding eggs in the 
patient's feces. 

Treatment 

The drug niclosamide or praziquantel will cure the 
infection. 

dishwasher detergent See alkaline corrosives. 
disulfiram See Antabuse. 



diuretics These are the most commonly pre- 
scribed drugs for the treatment of high blood pres- 
sure. The four types of diuretics are thiazide and 
thiazidelike, loop, potassium-sparing, and combina- 
tion. Each type works by affecting a different part of 
the kidneys and may also have different uses, side 
effects, and precautions. Overdoses are not gener- 
ally harmful; more serious are the adverse effects 
from chronic use or misuse. Examples of some 
of the drugs within each diuretic type are thia- 
zides (chlorthalidone, hydrochlorothiazide, meto- 
lazone; loop (bumetanide, furosemide, torsemide); 



92 DMSA 



potassium-sparing (amiloride, eplerenone, spirono- 
lactone, triamterene); and combination (amiloride 
and hydrochlorothiazide, spironolactone and 
hydrochlorothiazide, and triamterene and hydro- 
chlorothiazide). Because the potassium-sparing 
diuretics are not very effective alone, they are often 
combined with another diuretic. 

Symptoms 

Lethargy, weakness, and dehydration, which may 
be delayed for two to four hours until the diuretic 
action begins. The diuretic spironolactone may not 
produce symptoms until the third day; thiazide 
diuretics may cause hyperglycemia. 

Treatment 

There are no specific antidotes; treatment is symp- 
tomatic. Replace fluid loss and correct electrolyte 
abnormalities; monitor potassium levels. Induce 
vomiting or perform gastric lavage followed by 
activated charcoal and a cathartic (unless the 
patient is dehydrated). 

DMSA (Meso-2,3-dimercaptosuccinic acid) This 
chelating agent (also known as succimer) is a com- 
monly used drug for reducing toxicological effects 
of lead and methylmercury poisoning. DMSA is 
currently the only approved oral medication in the 
United States for children with high levels of lead. 
It works by chemically binding with lead in the 
patient and removing the poison from the body. 

dog button plant See nux-vomica. 

dog hobble (Leucothoe) [Other names: dog laurel, 
fetterbush, pepper bush, sweet bells, switch ivy, 
white osier.] This deciduous or evergreen shrub 



grows from Virginia to Florida, Tennessee, Louisi- 
ana, and California. Its white or pink flowers grow 
in clusters. 

Poisonous part 

The leaves and nectar (in honey) are toxic and con- 
tain the toxin grayanotoxin (andromedotoxin). 

Symptoms 

Burning in the mouth, followed gradually by 
increased salivation, diarrhea, and prickly skin; 
headache, vision problems, bradycardia, severe 
hypotension, and possibly convulsions and 
coma. 

Treatment 

Fluid replacement, atropine for bradycardia; ephed- 
rine for hypotension that does not respond to fluid 
replacement. 

drain cleaners See alkaline corrosives. 



dyphylline (7-dihydroxypropyltheophylline) One 

of the group of bronchial tube relaxers given 
to control asthma, bronchitis, and emphysema, 
dyphylline was introduced in 1946 and is available 
in time-release tablets or syrup. 

Symptoms 

Within one hour, overdose produces headache, 
nervousness, insomnia, nausea, vomiting, rapid 
heartbeat, low blood pressure, convulsions, and 
circulatory failure. 

Treatment 

Perform gastric lavage, followed by symptomatic 
treatment. 

See also bronchial tube relaxers. 



E 



E. coli 01 57:H7 The most deadly of the hundreds 
of strains of Escherichia coli, this type of E. coli has been 
recognized as a cause of foodborne illness leading to 
kidney failure and death since 1982. It's known 
popularly as "the hamburger disease" because of its 
links with undercooked fastfood hamburgers. 

Although most strains of E. coli are harmless and 
live in the intestines of both humans and animals, 
the 0157:H7 strain produces a powerful toxin 
that can cause severe illness. An estimated 70,000 
cases of infection occur in the United States each 
year. Most illness has been associated with eating 
undercooked, contaminated ground beef. Other 
outbreaks have been traced to many different 
types of food. E. coli has been discovered surviving 
in dry fermented meat and salami despite produc- 
tion standards that meet federal and industry food 
processing requirements. It has also been found in 
unpasteurized milk, cider, and apple juice, in let- 
tuce, and in untreated water. 

It's especially common in day care centers and 
among toddlers who are not yet toilet trained. 
Patients are infectious for about six days while 
bacteria are excreted in their stool. There is no 
solid evidence, but it appears that victims can get 
this infection more than once. Most states now 
ask doctors to report outbreaks of the disease, but 
none regularly tests for other strains of E. coli that 
produce the toxin. 

Symptoms 

The toxins cause severe cramps and watery or 
bloody diarrhea lasting for 6 to 8 days. Other 
symptoms include nausea and vomiting appearing 
within hours to a week after eating, but not usually 
any fever. Most people recover quickly and com- 
pletely, but the complications are what make this a 
serious disease (see "Complications"). 



Diagnosis 

Identification of the bacterium in stool. Most labs 
that culture stool don't test for E. coli 0157:H7, so 
it's important to request that the stool be tested 
for this organism. Everyone with sudden bloody 
diarrhea should have the stool checked for this 
bacterium. 

Treatment 

Most patients recover within 10 days without spe- 
cific treatment. There is no evidence that antibiot- 
ics help and some evidence to suggest it may trigger 
kidney problems. Antidiarrhea medicine should 
also be avoided. Hemolytic uremic syndrome (see 
under Complications), on the other hand, is a life- 
threatening condition that is treated in a hospital 
intensive care unit, with blood transfusions and 
kidney dialysis. 

Complications 

In certain people (the very young or old), the 
bacteria may cause hemolytic uremic syndrome 
(HUS), a condition in which the red blood cells are 
destroyed and the kidneys fail. Between 2 and 7 
percent of infections lead to this complication. In 
the United States, HUS is the main cause of kidney 
failure in children. There is no cure. Adults may 
develop an extremely serious bleeding disorder 
called thrombotic thrombocytopenic purpura in 
which blood stops clotting, small red spots and 
large bruises appear all over the body, and blood 
oozes through the mouth. 

Patients with only a mild infection usually 
recover completely. Of those who develop HUS, 
one-third have abnormal kidney function years 
later, and a few need long-term dialysis. Another 
8 percent suffer with other comphcations such 
as high blood pressure, seizures, bhndness, and 



93 



94 ecstasy 



paralysis for the rest of their lives. Even with inten- 
sive care, the death rate from HUS is between 3 
percent and 5 percent. In addition, the outlook is 
not promising for adults who develop thrombotic 
thrombocytopenic purpura. 

ecstasy Also known as methylenedioxymeth- 
amphetamine (MDMA), ecstasy is a synthetic, 
psychoactive drug that is chemically similar to 
methamphetamine and the hallucinogen mes- 
caline. It is taken as a capsule or tablet and was 
initially popular among white adolescents and 
young adults who took it at all-weekend parties 
(raves) and at dance clubs. Use has now expanded 
to include other ethnic groups and gay males. The 
attraction is the feeling of euphoria, emotional 
warmth, and distortions in tactile experiences and 
time perception that the drug causes. Acute, nega- 
tive effects of ecstasy begin about 30 minutes after 
oral intake. Within 60 minutes, however, the jaw 
clenching, dry mouth, blurry vision, and sweating 
give way to feelings of relaxation. The effects pla- 
teau for up to 90 minutes and then diminish over 
three to four hours. As users come down from their 
high, some take additional ecstasy to prolong the 
effect, and this practice can lead to serious, life- 
threatening effects. 

Ecstasy affects the brain by binding to the trans- 
porter for the brain chemical called serotonin, 
which plays a critical role in regulating mood, 
sexual activity, sleep, aggression, and sensitivity to 
pain. The drug is also addictive for some people. 
A survey of ecstasy users found that 43 percent 
met the diagnostic criteria for dependence, and 
these results are similar to those found in other 
countries. 

Symptoms 

Ecstasy can produce confusion, memory prob- 
lems, increases in heart rate and blood pressure, 
blurry vision, nausea, chills, sweating, depression, 
sleep problems, drug craving, and severe anxiety. 
These symptoms can occur soon after taking the 
drug or even days or weeks later. In high doses, 
ecstasy can disrupt the body's ability to regulate 
temperature and may cause hyperthermia, which 
then can result in liver, kidney, and cardiovascular 



system failure and death. In fact, most ecstasy- 
related deaths are caused by hyperthermia and 
heat stroke. Animal research showed that expo- 
sure to ecstasy for only four days caused damage 
to serotonin nerve terminals that was still evident 
up to seven years later. Symptoms associated 
with withdrawal from the drug include fatigue, 
loss of appetite, depressed feelings, and difficulty 
concentrating. 

Treatment 

Management of ecstasy overdose/poisoning is 
similar to that for amphetamines. The individual 
should be checked for clear airways, breathing, 
and circulation, as well as hypertension and ven- 
tricular dysrhythmias. Activated charcoal should be 
administered and symptoms should be managed, 
including oxygen and intravenous fluids for hypo- 
tension; benzodiazepines for agitation or seizures; 
dopamine or norepinephrine for hypotension that 
does not respond to fluid; lidocaine for ventricular 
dysrhythmias; correction of electrolyte abnormali- 
ties; and other measures as needed. 

edrophonium chloride Antidote used in the 
treatment of curare poisoning reversing the neu- 
romuscular blockade produced by curare, tubocu- 
rarine, or gallamine. It also treats the respiratory 
depression caused by curare overdose. It must be 
used with caution, however, among patients with 
chronic lung disease and heart problems. 
See also curare. 



elderberry, black and scarlet elders (Sambucus 
canadensis and S. pubens) [Other names: Ameri- 
can elder, sweet elder.] Often cultivated for its 
ornamental foliage, this indigenous shrub is found 
throughout the United States and Canada in low, 
damp ground and waste places. The elderberry 
grows from five to 12 feet with a rough gray bark 
and a faintly sweet odor. It flowers in June and 
July with white, star-shaped clusters; its black ber- 
ries mature in September and October. Sometimes, 
flower and fruit appear at the same time. The Euro- 
pean elder is larger than its American cousin but is 
otherwise quite similar. 



ergot 95 



Poisonous part 

The entire plant is toxic, although the ripe fruit 
is edible when cooked, and in limited amounts 
it may not cause symptoms even if eaten raw. 
According to some sources, the flowers are prob- 
ably nontoxic and the berries cause nausea only if 
eaten raw in large numbers. The poison is cyano- 
genic glycosides found mostly in the roots, stems, 
and leaves and an unidentified cathartic mostly in 
the bark and roots of some species. Proper cooking 
destroys the toxic principle. Children have been 
poisoned by eating the roots or using the pithy 
stems as blowguns. 

Symptoms 

Eating leaves, bark, root, or immature berries may 
cause serious diarrhea. Juice from the berries of S. 
mexicana has caused nausea, vomiting, and cramps 
within 15 minutes, dizziness, numbness, and stu- 
por. At least one anecdotal case of cyanide poison- 
ing in humans from this plant has been recorded. 

Treatment 

Administer fluids. 

See also cyanogenic glycosides. 

endrin [Trade names: Compound 269, Experimen- 
tal Insecticide 269.] A highly toxic chlorinated 
hydrocarbon insecticide and rat poison, endrin 
has been responsible for numerous fatalities. This 
white crystalline solid can be inhaled, ingested, or 
absorbed through the skin. 

Symptoms 

Between 30 minutes and 10 hours after ingestion, 
symptoms appear including giddiness, weakness, 
nausea, confusion, insomnia, lethargy, repeated 
convulsions, and loss of consciousness followed by 
respiratory failure and death. 

Treatment 

There is no specific antidote. Perform gastric lavage 
but do not induce vomiting because of the risk 
of sudden onset of seizures; administer activated 
charcoal and a cathartic. Irregular heartbeat may 
respond to propranolol. 

See also chlorinated hydrocarbon pesticides. 



ephedrine A potent central nervous system stim- 
ulant used to treat low blood pressure following 
overdose with antihypertensive drugs such as beta 
blockers, calcium channel blockers (verapamil, 
nifedipine), vasodilators (minoxidil, prazosin), etc. 
See also beta adrenergic blockers. 

epinephrine This catecholamine produced natu- 
rally in the body is used to treat anaphylaxis or car- 
diac arrest. It may also be helpful in raising low blood 
pressure resulting from an overdose of beta adrener- 
gic blockers and other heart-depressant drugs. 
See also beta adrenergic blockers. 

ergot (Claviceps purpurea) This parasitic fungus 
is found primarily in rye grain, which can also 
contaminate flour made from the grain. Ergot 
poisoning can occur after eating rye meal or bread 
that has been prepared from the contaminated 
grain. Originating in Europe, ergot is now found 
throughout the world. 

Ergot poisoning was epidemic during the Middle 
Ages, when 40,000 Frenchmen died from "St. 
Anthony's Fire." It is no longer a danger today 
because of widespread screening programs used to 
check cereal grains for the fungus. 

Ergot was used in earlier tunes as an abortifa- 
cient because of its ability to contract the uterus; 
however, doses necessary to expel the uterine con- 
tents also tended to be fatal. In the 1 7th century, 
midwives used ergot to help the uterus contract 
after childbirth, and today it is still found in hospi- 
tals, where it is used for the same purpose. 

Symptoms 

Drowsiness, headache, giddiness, nausea, vomiting, 
cramps, itching, and respiratory and cardiac arrest. 
In severe poisoning cases, gangrene involving the 
fingers, toes, ears, and nose may occur. Ingestion 
can also cause painful convulsions, permanent dam- 
age to the central nervous system, and psychosis. 

Treatment 

Gastric lavage followed by activated charcoal, 
together with symptomatic and supportive treatment. 
Amyl nitrate is sometimes used to ease spasms. 
See also nitroglycerin. 



96 Escherichia coli 



Escherichia coli See E. coli 0157:H7. 

ethanol The alcohol in alcoholic drinks; ethanol 
is administered either intravenously or orally to 
treat methanol or glycol poisonings. 

See also isopropyl alcohol; methyl alcohol. 



ether (diethyl ether) The first general anesthetic, 
ether was first demonstrated successfully in Boston 
in 1846, when a tooth was extracted without pain 
while the patient was breathing ether. Soon after, 
the anesthetic properties of chloroform and nitrous 
oxide were added to the anesthesiologist's arsenal. 

A colorless liquid, ether is administered on a 
gauze mask over a patient's nose and mouth and 
produces unconsciousness when inhaled. It is so 
flammable that even static electricity can cause an 
explosion. For this reason, ether was abandoned 
after the 1930s when it was replaced by other, safer 
anesthetic agents. 

Symptoms 

Overdose depresses the central nervous system and 
stops breathing. 

Treatment 

Remove the gas and force ventilation, maintain 
breathing and keep warm to avoid shock. If a high 
fever develops, pack the body in wet towels or 
administer dantrolene sodium and procainamide. 

See also anesthetics, gaseous/volatile; chlo- 
roform; NITROUS OXIDE. 

ethyl alcohol Another name for ethanol, the 
alcohol in alcoholic drinks. It is used as an antidote 
to antifreeze poisoning. 

See also antifreeze; isopropyl alcohol. 

ethylene chlorohydrin This colorless, odorless 
liquid is used as an industrial solvent and to 
facihtate seed germination. It evaporates quickly 
at room temperature. Because it has no smell and 
does not irritate the mouth or nose, it is possible to 
become exposed before danger is realized. 



Symptoms 

In the wake of continued exposure, ethylene chlo- 
rohydrin is a central nervous system depressant 
and damages the heart, lungs, liver, and kidneys. It 
is not yet certain whether it causes cancer or fetal 
damage. Symptoms appear soon after exposure, 
including nausea, vomiting, headache, vertigo, 
delirium, low blood pressure, slow breathing, cya- 
nosis, and coma. Death occurs from respiratory 
and circulatory failure. In addition, there have 
been reports of impaired DNA and possible birth 
defects. 

Treatment 

Move the victim into fresh air and remove afl 
contaminated clothing. Perform artificial respira- 
tion or administer oxygen as needed. For inges- 
tion, perform gastric lavage followed by a saline 
cathartic. Do not administer epinephrine or other 
stimulants. 



ethylene dibromide (EDB) This volatile liquid 
is used in antiknock gasoline mixtures, especially 
aviation fuel, and as a pesticide and fumigant for 
soil, fruits, and vegetables. It can cause chemical 
burns or (if inhaled) respiratory tract irritation 
and pulmonary edema. Its use as a pesticide has 
been restricted since 1984 because of its suspected 
carcinogenic role. In cases of inhalation poisoning, 
rescuers must wear breathing apparatus and pro- 
tective clothing to avoid exposure. Once absorbed 
in the body, EDB can disrupt cell metabolism and 
initiate multisystem failure throughout the body. 

Symptoms 

If inhaled, EDB can irritate the eyes and upper 
respiratory tract; pulmonary edema is found within 
six hours but may take as long as two days to 
develop. Ingestion causes vomiting, diarrhea, cen- 
tral nervous system depression, seizures, and meta- 
bolic acidosis. In fatal cases, there is acute kidney 
failure, liver damage, and muscle necrosis. Inges- 
tion of 4.5 ml of hquid EDB can be fatal. 

Treatment 

There is no specific antidote. Treat symptoms, and 
provide oxygen if needed. For skin/eye contami- 



exotoxin 97 



nation, remove clothes and wash with soap and 
water; irrigate eyes with saline or tepid water. 
For ingestion, do not induce vomiting because 
of corrosive effects and danger of rapid onset of 
coma or seizure. Perform gastric lavage followed 
by the administration of activated charcoal and a 
cathartic. 

See also pesticides. 



ethylene glycol See antifreeze. 

eucalyptus (Eucalyptus globulus Labill) Also 
known as a gum tree, this genus includes more 
than 600 species (both trees and shrubs) in the 
myrtle family. It is the essential oils of this tree that 
can be toxic. The eucalyptus is native to Australia, 
New Zealand, Tasmania, and nearby islands and 
is cultivated throughout the temperate regions of 
the world as shade trees or in forestry plantations. 
About 90 species are grown in California, and a few 
are found in Florida. 

The bark of the eucalyptus tree is distinctive, 
peeling off in long strips exposing the inner layer. 
Leaves are leathery and smooth, and the flower 
petals (white, yellow, or red) form a cap when the 
flower expands and attract honeybees. The fruit is 
surrounded by a woody, cup-shaped receptacle and 
contains many tiny seeds. 

Poisonous part 

The leaf glands of many species contain a volatile 
aromatic oil known as eucalyptus oil, and is an 



active ingredient in expectorants and inhalants. 
IX contains 70 percent eucalyptol; the toxic dose 
is 5 ml. 

Symptoms 

Following an acute overdose by mouth, symptoms 
may appear within five to 30 minutes and include 
burning in the mouth and throat followed by nau- 
sea and vomiting. Drowsiness, confusion, restless- 
ness, delirium, muscle twitching, and coma may 
follow. Death may occur as a result of depression 
of the central nervous system and respiratory 
arrest. 

Treatment 

Treat seizures and coma if they occur. There is no 
specific antidote. Perform gastric lavage but do not 
induce vomiting because of the risk of inducing 
seizures. Administer activated charcoal. 



exotoxin Exotoxins include some of the most 
poisonous substances known, which are released 
by some types of bacteria into the bloodstream. 
Tetanus and diphtheria bacilli produce some of the 
best-known exotoxins; the former affects the ner- 
vous system and causes muscle spasms and paraly- 
sis, and the latter damages the heart and nervous 
system. Vaccinations for some of the potentially 
fatal bacterial diseases use detoxified exotoxins to 
prevent the disease. Once infection has occurred, 
however, treatment includes antibiotics and an 
antitoxin to neutralize the exotoxin. 
See also toxoid. 



F 



false Jerusalem cherry (Solanum pseudocapsicum) 

This decorative pot plant has spread through 
cuhivation from its native Gulf Coast region and 
Hawaii. It is a member of a very large genus with 
1,700 species, most of which have not been evalu- 
ated toxicologically. 

Poisonous part 

Human poisoning is usually attributed to imma- 
ture fruit, which contains the toxin solanine 
glycoalkaloid. 

Symptoms 

While there is little danger of fatal poisoning in 
adults, children may ingest a fatal amount of this 
plant. Symptoms appear several hours after inges- 
tion and include gastric irritation, scratchy throat, 
fever, and diarrhea (solanine poisoning is often 
confused with bacterial gastroenteritis). 

Treatment 

Provide the same general supportive care that would 
be given in gastroenteritis cases; fluid replacement 
may be required. 

false morel See turbantop. 



fenoprofen See nonsteroidal anti-inflammatory 

DRUGS. 



fentanyl See narcotics. 

fer-de-lance This extremely venomous pit viper 
lives in cultivated lands and tropical forests of cen- 



tral Mexico into South America. A member of the 
viper family, it is considered a pit viper because of 
its sensory pit between each eye and nostril. 

The fer-de-lance is gray or brown with black- 
edged diamonds on a lighter border and is found 
in tropical America ranging from farms to tropical 
forests. Its name (French for "lancehead") is some- 
times used to refer collectively to all snakes of the 
Central and South American genus Bothrops and 
the Asian genus Trimeresurus, and it is called barba 
amarillo ("yellow chin") in Spanish. Other pit viper 
relatives include the dangerous South American 
wutu (Bothrops alternatus), the jumping viper or 
tommy-goff (B. nummifera) of Central America, 
the Okinawa habu (Trimeresurus flavoviridis) found 
in the Ryukyu Islands, and Wagler's pit viper (T. 
Wagleri). 

Symptoms 

With a bite from this viper, blood cannot coagulate 
and hemorrhages into muscles and the nervous 
system. There is local pain, bleeding from the bite, 
gums, nose, mouth, and rectum. Shock and respi- 
ratory arrest are followed by death. 

Treatment 

Antivenin is available. 

See also antivenin; pit vipers; snakes, 

POISONOUS. 



fertilizers Plant foods that contain one of three 
ingredients necessary for plants to grow: potas- 
sium, nitrogen, or phosphorous. They are not gen- 
erally considered particularly toxic even if ingested 
by children, unless the fertilizer also contains herbicides 
or insecticides. If a child ingests products contain- 
ing only these three ingredients, usually the only 



98 



first aid 99 



symptoms that occur will be vomiting or diarrhea. 
However, many fertilizers also contain additives 
that could be toxic. 

See also herbicides; insecticides. 

fire ant (Solenopsis) Several species of these 
small, aggressive ants, also known as thief ants, are 
found in North America. These red or yellow ants 
live in loose mounds with open ventilation craters 
and long tunnels, usually located in meadows of 
clover and Bermuda grass and in row crops; they 
occasionally invade homes. 

Poisonous part 

The release of histamine causes the painful symp- 
toms common in fire ant stings. 

Symptoms 

A sting from the fire ant can cause severe pain, 
swelling, itching, reddening, warmth, and burning. 
Blisters may form and they are prone to infection 
if broken. 

Treatment 

Ice, compresses, and cleansing of the wound to 
prevent infection. Neither antihistamines, cortico- 
steroids, nor antibacterial ointments significantly 
ease symptoms. 

fireworks According to federal regulations, all 
fireworks must be sealed to prevent leakage of 
gunpowder during shipment and handhng and 
must be constructed to prevent burnout through 
the sides or blowout through the bottom of the 
device after ignition. Still, each year fireworks 
injure many thousands of Americans, usually chil- 
dren and teenagers. These products are also toxic 
if ingested. 

Gold sparklers may contain barium nitrate, 
paste, chalk, dextrin, iron, and aluminum; green 
sparklers contain barium nitrate, potassium per- 
chlorate, wheat pastes, gum, dextrin, and alu- 
minum powder. Red sparklers contain strontium 
carbonate, nitrate, and potassium perchlorate, 
plus gums, wheat pastes, dextrin, and aluminum 
powder. 



Symptoms 

If ingested, the soluble barium salts contained in 
these products can cause vomiting, abdominal 
pain, bloody diarrhea, shallow breathing, convul- 
sions, coma, and death from respiratory or cardiac 
failure. Strontium may cause vomiting, abdominal 
pain, bloody stools, and methemoglobinemia; per- 
chlorates may cause vomiting, abdominal pain, and 
methemoglobinemia. 

Treatment 

When a sparkler has been eaten, induce vomiting 
or perform gastric lavage; in the case of nitrate- 
induced methemoglobinemia, intravenous solution 
of I percent methylene blue is recommended. 

first aid It is not always easy to know whether 
someone is the victim of poisoning or has the signs 
and symptoms of conditions that mimic poison- 
ing, such as seizures, stroke, insulin reaction, and 
alcohol intoxication. Some signs and symptoms of 
poisoning include 

• Redness or burns around lips and mouth, which 
may occur when certain poisons are ingested 

• Burns, odors, or stains on the individual, the 
clothing, furniture, floor, rugs, or other objects 
in the surrounding area 

• Breath that smells like chemicals 

• Vomiting, breathing problems, confusion, exces- 
sive sleepiness, or other unexplained signs 

• Empty medication bottles or scattered pills 

If you suspect poisoning, check for the signs and 
symptoms but also contact the poison control cen- 
ter at 800-222-1222 before you give anything to 
the affected individual. You can also call 911 for 
emergency help or if you don't know the number 
for the poison control center at the time of the 
poisoning. Below are the recommended actions to 
take for different types of poisoning situations. 

Inhaled Poisons 

Immediately carry or drag the victim to fresh air. If 
you think you need protection, such as a respira- 
tor before you approach the victim, call the fire 



100 fish contamination 

department and wait for emergency equipment to 
arrive. 

After you find the victim and move him or her 
clear of the affected area, do the following: 

• Check for breathing. If you are trained in CPR, 
try to resuscitate the individual. 

• Check the eyes and skin for chemical burns. 

• If there are burns on the skin, flush them thor- 
oughly with water. 

• Loosen tight clothing. 

• If the person's skin is blue or if the person has 
stopped breathing, give artificial respiration if 
you know how, and call rescue services. 

On the Skin 

If chemicals have splashed onto the skin, get 
the victim away from the poisonous substance. 
Remove contaminated clothing and flood the skin 
and hair with soap and water for at least 1 5 min- 
utes. Seek medical treatment. Later, throw away 
the contaminated clothes or thoroughly wash them 
separately from other laundry. 

In the Eyes 

Eye membranes absorb pesticides and other chem- 
icals faster than any other external body part, and 
eye damage can occur in a few minutes with 
some types of chemicals. Therefore, it is critical 
to act immediately if poison has splashed into the 
eye(s): hold the eyelid open and wash quickly 
with clear running water from the tap or a gentle 
stream from a hose for at least 15 minutes. Do not 
use eye drops, chemicals, or drugs in the wash 
water as you cleanse the eye(s). If possible, have 
someone else contact poison control while you 
help the victim. 

Stings 

• Remove the stinger by scraping with a hard, flat 
object, hke a credit card or the back of a knife. 

• Apply cold towels or compresses to the sting 
site. 

• Position the bite area lower than the heart. 

• Be prepared to administer CPR. 



• In case of an allergic reaction (e.g., facial swell- 
ing, shock, breathing difficulties, abdominal 
pain), call 911. 

fish contamination High in protein, low in calo- 
ries, fat, and cholesterol — and widely suspected to 
fight against heart disease and cancer — this highly 
praised health food can also be a site of contamina- 
tion and spoilage. 

The problem is that fish readily soak up poi- 
sons and contaminants in water; tiny fish pick up 
contaminants from the plankton they feed on in 
polluted water, concentrating heavy metals (such 
as methyl mercury) in their organs. These fish 
are eaten by larger fish, further concentrating the 
toxins, and in big fish, such as swordfish and tuna, 
the contaminants may reach levels harmful to 
humans. 

Fatty fish like salmon, bluefish, and herring 
are vulnerable to chlorinated compounds such as 
PCBs, dioxins, and DDT, which linger in the body 
for years. Very minute quantities of these sub- 
stances in the water will produce very high con- 
centrations in fish. 

One of the more insidious types of mercury 
poisoning occurs through the contamination of 
fish in lakes and streams throughout the United 
States as a result of extensive agricultural fungi- 
cide and pesticide use and the industrial by-prod- 
ucts of chlorine production. Estimates suggest up 
to 10,000 tons of mercury infiltrates the sea each 
year; once in the water, it enters the food chain 
where it is converted into organic methyl mer- 
cury, one of the most toxic substances known. 
The presence of sewage in the water facilitates 
this deadly conversion by bacteria living in the 
mud; once it occurs, the contaminated bacteria 
are then eaten by plankton, which are in turn 
eaten by pike, pickerel, perch, walleye, muskie, 
and white bass. 

Unlike inorganic mercury compounds, methyl 
mercury is hard to detect in the blood; it does 
not readily break down in the body and can take 
months to be excreted. In addition, it can pass eas- 
ily through the blood-brain barrier, irreversibly 
damaging brain cells; it also crosses the placenta 
and builds up in the fetal brain and blood. Methyl 



fish contamination 101 



mercury seems to affect women more tfian men, 
and cfiildren and infants most of all. 

The first cases of contaminated fish poisoning 
occurred in Japan in 1953 and 1970, when more 
than 121 cases — and 46 deaths — were reported. At 
that time, methyl mercury chloride flowed directly 
into a bay and river near a manufacturing plant. 

According to research conducted in the 1970s, 
fish in the Great Lakes were also contaminated with 
methyl mercury (2.8 parts per million). Today, the 
Food and Drug Administration mandates that tuna 
must contain less than 0.5 mg/kg, but scientists esti- 
mate that to be safe, humans should ingest no more 
than 0.1 mg of mercury per day; if a fish contains 
1 parts per billion of mercury, then the safe weekly 
limit would be about three portions of fish a week 
{Wi lb.). Still, no methyl mercury fish poisonings 
have been reported since Japan's incidences. 

Low levels of mercury in fish may not be as 
harmful to regular fish eaters as experts once 
thought, according to a recently released study. 
Heavy consumption of mercury-tainted fish has 
long been considered particularly dangerous to 
pregnant women and their unborn babies. But in 
a new study conducted by the University of Roch- 
ester over a period of 15 years in the Seychelles 
islands, tests show no link between the children's 
development over their first five and a half years 
and the levels of mercury found in their mother's 
hair during pregnancy. (Concentration of mercury 
in the mother's hair is a measure of the amount of 
mercury to which fetuses were exposed.) 

The journal Neurotoxicology published 11 articles 
on the study, which tracked the mental and physical 



development of more than 1,500 children starting at 
six months of age. The study is expected to sharpen 
the debate over mercury poisoning in the United 
States, where 37 states advise people to limit con- 
sumption of freshwater fish because of mercury. 

There is very little known about ways to remove 
the methyl mercury pollutants from contaminated 
water, which may remain poisoned for between 10 
and 100 years. 

Fish spoilage 

The danger of fish contamination is not just with 
the contaminants they ingest. Because bacteria that 
live on fish are adapted to withstand the cool and 
cold waters of lakes and oceans, they can thrive in 
temperatures cold enough to preserve other food. 
These microbes will quickly spoil the fish, unless 
it is kept at temperatures close to freezing. Even 
under the best conditions, fish lasts only seven to 
12 days; but it often takes seven days for fish to get 
from the water to the supermarket, where it may 
sit for several more days. 

How to protect against contamination 

Seafood should look and smell fresh, with vivid 
skin and bright eyes and no fishy or ammonia 
odor. It should be displayed on ice in the store; 
otherwise, fish is best selected from the bottom 
of the refrigerator case where it is coldest. Once 
home, it should be kept very cold and eaten within 
one or two days. Cook thoroughly, but no amount 
of cooking will destroy contaminants. Scrape off 
the fatty skin before cooking. Pregnant women, 
nursing mothers, and young children should limit 



FISH AND SHELLFISH POISONING 



Type 


Onset 


Fish/Shellfish 


Effects 


Ciguatera 


one to six hrs. 


Barracuda, grouper, red snapper 


Gastroenteritis, hot and cold reversal, 
weakness, myalgia 


Scombroid 


Immediate to delayed 


Tuna, mahimahi, mackerel, 
bonita 


Gastroenteritis, flush, wheezing, rash 


Neurotoxic shellfish 


Up to three hrs. 


Mussels 


Gastroenteritis, ataxia, paresthesias 


Paralytic shellfish 


Within 30 min. 


Mussels, clams, "red tide" 


Gastroenteritis, ataxia, respiratory 
paralysis 


Tetroclotoxin 


30-40 min. 


Pufferfish, sunfish, porcupine 
fish, California newt 


Vomiting twitches, weakness, respiratory 
paralysis 



102 flea and tick killers 



consumption of fish that might have high levels of 
mercury and PCBs. 

flea and tick killers See organophosphate 

INSECTICIDES. 

floor polish and wax See petroleum distillates. 

Flumazenil This nontoxic drug is used to rapidly 
reverse a coma brought on by benzodiazepine 
overdose. After intravenous administration, the 
reversal takes effect within two minutes. 
See also benzodiazepines. 



flunitrazepam [street names: roofies, rophies, 
forget-me pill, circles, Mexican valium, rib, roach-2, 
roonies, rope, ropies, ruffles, roaches] A sleeping 
pill prescribed for insomnia in Mexico, Europe, 
Asia, and South America, flunitrazepam (Rohyp- 
nol) has not been approved for use in the United 
States. This benzodiazepine is effective for short- 
term treatment of insomnia and as a sedative hyp- 
notic and preanesthetic drug. The effects of the 
drug are similar to those of diazepam (Vahum), 
although flunitrazepam is about ten times more 
potent. Because the drug cannot be detected by 
routine benzodiazepine screens, it can be used by 
people who want to become intoxicated but avoid 
driving-under-the-influence charges. 

In the United States, flunitrazepam is often used 
along with alcohol, which results in a synergistic 
effect and produces disinhibition and amnesia. 
This combination, along with the fact that the drug 
is inexpensive (typically less than five dollars per 
tablet) has made flunitrazepam popular as a date 
rape drug. Perpetrators slip a tablet into the drink 
of their intended victim, and the drug, which is 
colorless, odorless, and tasteless, dissolves quickly. 
When flunitrazepam is taken along with alcohol or 
other drugs (e.g., marijuana, cocaine), sedation can 
occur as soon as 20 minutes after ingestion. The 
drug's effects will peak within two hours and can 
impair judgment and motor skiHs and cause black- 
outs that can last eight hours or longer, depending 
on the dosage. 



Cases of date rape have been reported across 
the United States, primarily on college campuses, 
in which victims — usually women — wake up in 
unfamiliar surroundings with no memory of what 
occurred in the preceding hours. Although most 
cases are reported by women, flunitrazepam has 
the same effect on men. 

In March 1995, flunitrazepam was classified as 
a Schedule III drug by the World Health Organiza- 
tion. Based on an increase in abuse of the drug in 
the United States, however, the Drug Enforcement 
Agency is considering making flunitrazepam a 
Schedule I drug — a high potential for abuse, with 
no currently accepted medical use in treatment, 
and lacking accepted levels of safety for use under 
medical supervision. 

Symptoms 

In addition to impaired judgment and motor skills, 
symptoms include visual disturbances, drowsiness, 
confusion, decreased blood pressure, gastrointesti- 
nal disturbances, urinary retention, and memory 
impairment. When combined with alcohol, fluni- 
trazepam may cause aspiration, respiratory depres- 
sion, and death. 

When dependence develops, withdrawal symp- 
toms can include headache, muscle pain, extreme 
anxiety, tension, restlessness, confusion, and irrita- 
bility, along with delirium, hallucinations, tingling 
of the extremities, convulsions, shock, and cardio- 
vascular collapse. 

Treatment 

As is necessary with other benzodiazepines, treat- 
ment for flunitrazepam dependence must be done 
gradually with use tapering off. If alcohol and 
flunitrazepam have been used together, treatment 
may need to include additional medication for 
alcohol withdrawal. Once patients receive their 
initial phenobarbital doses, a benzodiazepine such 
as diazepam or lorazepam may be given to alleviate 
emerging alcohol withdrawal symptoms. 

fluoride Fluoride poisoning is usually caused by 
the accidental ingestion of roach powder insecti- 
cides, although it can also occur in children who 
eat large amounts of vitamin-fluoride tablets or too 



flyagaric 103 



much fluoride toothpaste. The recommended dose 
of fluoride for children under age two is 0.25 mg/ 
day; vitamin -fluoride tablets contain 1 mg, as does 
the average amount of toothpaste on a toothbrush. 
If too much toothpaste is swallowed by a child in 
one day, it could result in fluoride poisoning and 
severe mottling of the tooth enamel. For this rea- 
son, new research suggests children under age two 
should brush without toothpaste; those between 
ages two and five should be given toothpaste 
no larger than a pea and required to rinse their 
mouths thoroughly after brushing. 

In addition, the American Dental Association 
Council of Dental Therapeutics suggests that fluo- 
ride supplements prescribed by pediatricians should 
be hmited to those children whose drinking water 
has a fluoride concentration less than 70 percent 
of the one-part-per-million level recommended 
for community water. Still, fluoride is an effective 
weapon against the development of dental cavities 
and should not be abandoned because of potential 
problems. 

The most famous case of fluoride poisoning 
occurred at the Oregon State Hospital in 1943, 
when workers accidentally mixed 1 1 pounds of 
fluoride sodium salt with 10 gallons of scrambled 
eggs, killing 47 of the 263 patients who ate the 
tainted breakfast. 

Symptoms 

Following ingestion, symptoms include pain, sali- 
vation, nausea, vomiting, and diarrhea. Vomiting 
and diarrhea usually get rid of most of the poison 
in the stomach, although the gastrointestinal tract 
readily absorbs fluoride salts. In the event of ingest- 
ing large amounts of fluoride, death from respira- 
tory paralysis can result within a few minutes. 
Death may also be caused by shock as a result of 
the effects of fluid loss from violent vomiting and 
the effects of the fluoride on the heart muscle, 
causing arrhythmias and heart failure. 

Although the lethal dose of sodium fluoride in 
adults is fairly large (5 grams), a fatal dose as low 
as two grams has been recorded. 

Treatment 

Intravenous glucose in isotonic saline in order to 
increase the amount of water in the urine secreted 



from the body is the most effective way of remov- 
ing fluoride from the body. Administer limewater, 
calcium chloride solution, or milk in order to bind 
as much fluoride ion as possible, followed by gastric 
lavage with any of the above fluids. This is followed 
by administration of calcium gluconate or calcium 
chloride to head off muscular spasms; calcium solu- 
tion should also be used to wipe away corrosive 
materials after being vomited or excreted. For hydro- 
fluoric skin bums, wash with cold water and admin- 
ister magnesium oxide. Treat shock as it occurs. 

fluoroacetate See compound 1080. 



fly agaric (yellow or red) (Amanita muscaria) 

Sometimes confused with its close relative, the 
panther mushroom (Amanita pantherina), this is 
a member of the poisonous Amanita mushroom 
genus that has been used for at least 3,000 years 
as an intoxicant in the rituals of many Asian and 
Indian tribes. Some mycologists believe it is the 
source of Soma, the mystical drug of the ancients. 
It gets its common name from its ancient use as a 
fly poison, since it attracts — and kills — any fly that 
lands on it. 

This mushroom is found in pastures and fields in 
summer throughout Europe and the United States 
in wooded areas and conifer forests, and some- 
times in open pastureland. It generally appears at 
the beginning and end of the summer months and 
in many places is more abundant than common 
edible mushrooms. 

Similar in appearance to the Amanita phalloides, 
the fiy mushroom cap ranges in color from yel- 
low, red, orange to deep brown, all with white 
warty patches on the caps that disappear as the 
mushrooms age. Because of its color variations, 
the panther mushroom is sometimes confused with 
the fiy agaric. Both varieties have the unattached, 
white gills with white spores that are typical of the 
Amanita genus. While both varieties are poisonous, 
the panther mushroom is the more deadly of the 
two. The taste is bitter and unpleasant. 

In most cases, people who have been poisoned 
by eating this mushroom have done so deliberately 
to experience hallucinations. 



104 fly mushroom 



Poisonous part 

The fly agaric and A. pantherina mushrooms con- 
tain the strong hallucinogen muscimol and the 
potent insecticide ibotenic acid. Despite its name, 
A. muscaria usually contains insignificant quantities 
of muscarine. 

Symptoms 

While poisoning is rarely fatal, severe symptoms 
appear quickly, between 30 minutes and three 
hours, and include severe gastrointestinal distress, 
drowsiness, lowered blood pressure, slow heart- 
beat, blurred vision, watery diarrhea, and intoxica- 
tion featuring euphoria and hallucinations. There 
may be intermittent drowsiness and manic behav- 
ior. In more severe cases, psychosis, convulsions, 
and coma can follow. 

Deaths have been reported in those whose 
immune systems were already compromised or in 
those who ate large amounts of the mushroom. 
Although deaths are rare in adults, they must be 
protected against injury during the manic phase 
of the intoxication. In preadolescents, however, 
ingestion of these mushrooms may cause convul- 
sions and coma. 

Treatment 

Vomiting soon after ingestion will lessen the sever- 
ity of symptoms. While some scientists have advo- 
cated the administration of atropine as a specific 
antidote, many others prefer to counteract delirium 
and coma with the use of physostigmine. 

See also Amanita mushrooms; mushroom poi- 
soning; PANTHER mushroom. 

fly mushroom See fly agaric. 

folic acid A B -complex vitamin that is very helpful 
in the treatment for methanol and ethylene glycol 
poisoning. Folic acid is essential for the synthesis of 
protein in the body and is believed to help eliminate 
the toxic metabolite formic acid from the body. 
See also methanol; vitamins. 

fomepizole A new drug approved in 1999 as a 
safe, effective antidote to antifreeze poisoning that 



offers advantages over other treatments and works 
extremely well. 

Automobile antifreeze consists almost entirely of 
ethylene glycol, a chemical that is harmless on its 
own. If swallowed, however, antifreeze is changed 
by the liver into dangerous substances that can lead 
to renal failure and death. Fomepizole works by 
blocking the liver enzyme that converts ethylene 
glycol into toxic substances. 

Antifreeze is usually ingested by mistake, as a 
suicide attempt or as a cheap substitute for ethanol. 
Experts estimate that there are about 5,000 cases 
of antifreeze ingestion each year in the United 
States. 

Previous treatments for antifreeze poisoning 
caused problems of their own. Before this treat- 
ment was approved, most patients were treated 
with high doses of ethanol (alcohol), which could 
lead to drunkenness, a dangerous drop in blood 
sugar level (hypoglycemia) or liver poisoning. 
Moreover, this type of treatment required intensive 
monitoring, and most of these patients required 
hemodialysis. 

The drug works better and has none of the 
complications associated with ethanol treatment, 
according to researchers. Still, about 17 patients in 
the most recent study of the new antidote needed 
hemodialysis. However, if the problem is caught 
early, treatment with this antidote should elimi- 
nate the need for hemodialysis. The new treatment 
may also be useful for pets who accidentally con- 
sume antifreeze. 

See also antifreeze. 



food poisoning Food poisoning and foodborne 
infections are caused by eating food that has been 
contaminated by toxic substances or bacteria that 
contain toxins. Researchers have identified more 
than 250 different diseases that can be caused by 
contaminated food or drink; most food items that 
carry disease are raw or undercooked foods of ani- 
mal origin, such as meat, milk, eggs, cheese, fish, 
or shellfish. 

Any illness that appears suddenly and within 
48 hours of eating questionable food and causes 
stomach pain, vomiting, and diarrhea should be 
treated as a case of food poisoning. Estimates of 



food poisoning 105 



the number of foodborne illnesses range from 
a low of 6 million to a high of 81 million cases 
yearly, with 9,100 deaths, according to the Cen- 
ters for Disease Control and Prevention (CDC). At 
least a third of these have been traced to poultry 
and meat. 

According to the Food and Drug Administra- 
tion, just about everyone experiences a foodborne 
illness at least once a year, whether they reahze it 
or not. The CDC estimates that 76 million cases of 
foodborne illness occur in the United States each 
year, and that most of these cases are mild and 
cause symptoms for only one or two days. The 
CDC also estimates that 325,000 people are hospi- 
talized and 5,000 people die each year because of 
foodborne illnesses. The most susceptible are the 
very young, the very old, and those that have a 
condition that compromises the immune system, 
such as HIV/ AIDS, cancer, or chronic fatigue syn- 
drome. Some foodborne diseases such as botulism 
or trichinosis are becoming less common, whereas 
others such as salmonellosis or E. coli infection are 
becoming more common. 

Types of food poisons 

Food can be affected by various contaminants, 
including bacteria, viruses, or parasites, all of 
which cause foodborne illness. Bacteria that may 
cause food poisoning include Campylobacter, Bacillus 
cereus, Clostridium perfringens, Listeria monocytogenes, 
Salmonella, Shigella, Staphylococcus aureus, Streptococ- 
cus A and D, Vibrio, and Yersinia. 

A surprising number of parasites contaminate 
undercooked and raw fish and shellfish, and may 
pose a health threat to anyone who eats them. 
They include a parasitic worm Anisakis simplex, 
Cryptosporidium, Cyclospora Diphyllobothrium latum. 
Entamoeba histolytica, Giardia, Nanophyetus salmincola 
or N. schikhobalowi. Toxoplasma gondii, and Trichi- 
nella spiralis. 

Seafood contaminated with toxins may look 
and taste normal, but standard cooking methods 
don't affect the toxin. State shellfish screening 
programs test shellfish for the presence of toxins 
and monitor the safety of shellfish harvest beds. 
However, people who catch their own shellfish 
from unapproved beds are at risk for various 
toxic infections. The toxins may be produced 



as fish spoil (as in scombrotoxin) or as the 
byproducts of toxic plankton (causing paralytic 
shellfish), or they may naturally be present in 
the fish itself (tetrodotoxin). They include cigua- 
toxin; paralytic, amnesic, diarrhetic, or neuro- 
toxic shellfish poisonings; scombroid poisoning; 
and tetrodotoxin. 

Food can also be contaminated by viruses, such 
as hepatitis A or the extremely common cahcivirus, 
or Norwalk-like virus, which is rarely diagnosed 
because the lab test for it is not widely available. 
Unlike many foodborne pathogens that have ani- 
mal reservoirs, it appears that the Norwalk-hke 
viruses are spread mainly from one infected person 
to another, especially among food handlers, includ- 
ing restaurant workers and food processors. Fungi, 
such as aflatoxins, and metallic contaminants, such 
as chlorinated compounds and mercury, can also 
cause food poisoning. 

Prevention 

The single most important way to prevent food- 
borne illness is thorough cooking, which kills most 
foodborne bacteria, viruses, and parasites. In addi- 
tion, proper food preparation, such as washing 
your hands, the cutting board, and knife with soap 
and water immediately after handling raw meat, 
poultry, seafood, or eggs, will help stop the spread 
of contamination. Anyone who is experiencing 
diarrhea or vomiting should not prepare food for 
others. 

To prevent the spread of foodborne diseases take 
the following steps: 

• Make sure food is thoroughly cooked or pasteur- 
ized; avoid eating raw or undercooked food from 
animal sources. 

• Keep the juices or drippings from raw meat, 
poultry, shellfish, or eggs separate from other 
food. 

• Do not leave potentially contaminated food for 
extended periods of time at room temperature. 

• Properly refrigerate leftovers and food prepared 
in advance of serving. 

• Keep the temperature in your refrigerator at 
40°F or below and 0°F in the freezer. 



106 food poisoning 



Allow air to circulate around refrigerated items, 
and always wrap food that is stored in a refrig- 
erator to keep out bacteria. 

Before and after preparing food, wash your hands 
thoroughly with soap and water to avoid con- 
tamination by Salmonella and other organisms. 

After using cutting boards and utensils, wash 
them thoroughly with hot soapy water before 
you allow any other food to touch them. Acrylic 
cutting boards are best because they can be put 
into a dishwasher and they resist cuts and pits 
where bacteria can hide. 

Thaw meat and poultry in a microwave oven or 
in the refrigerator and then cook them immedi- 
ately. Never thaw meat at room temperature. 

If you marinate meat or poultry, do not serve the 
marinade unless you cook it at a rolling boil for 
several minutes. 

Cook meat, poultry, and fish thoroughly and 
check the internal temperature using a meat 
thermometer. The thermometer should be 
placed into the thickest portion of the food and 
not touch bone. According to the CDC, the ther- 
mometer should register a minimum of 145°F 
for roasts and steaks, 165°F for poultry, and 
160°F for ground meat and pork. Juices should 
run clear when the food is pierced. 

Keep hot foods at 140-1 60°F until you serve 
them, especially those served in chafing dishes 
or warmers. Food should never be kept between 
40 and 140°F for more than two hours as this 
encourages bacterial growth. 

Serve meat, poultry, and fish on clean plates with 
clean utensils; do not use the plates and utensils 
you used to thaw or prepare the food. 

Cool poultry and meat quickly when refrigerat- 
ing leftovers. Do not let stuffed poultry stand for 
long periods. Do not refrigerate stuffed poultry: 
remove the stuffing and store it separately. 

Do not partially heat food and then finish cook- 
ing it later. This is an invitation for bacterial 
growth that might not be killed during subse- 
quent cooking. 

Never use cracked eggs because they may con- 
tain Salmonella. However, even uncracked eggs 



SAFE FOOD STORAGE 

Basic Guidelines by the U.S. Department of Agriculture 
and the Food Marketing Institute 



Food 



Where 



How Long 



Poultry 

Raw 



Cooked 

Seafood 

Lean fish, raw 

Fatty fish, raw 
Raw shrimp 
Cooked seafood 



Meat 

Ground meat 



Chops (all) 
Lamb chops 
Pork chops 

Roasts (all) 
Beef roasts 
Veal/pork roast 
Lamb roast 

Steak 

Cooked leftovers 

Luncheon meats 
Unopened 
Opened 



Dairy 

Raw eggs in shell 
IHard-boiled (in shell) 
Milk 

Mayonnaise (opened) 



Refrigerator 
Freezer 
Refrigerator 
Freezer 

Refrigerator 

Freezer 

Refrigerator 

Freezer 

Refrigerator 

Freezer 

Refrigerator 

Freezer 

Refrigerator 

Freezer 

Refrigerator 

Freezer 

Freezer 

Refrigerator 

Freezer 

Freezer 

Freezer 

Refrigerator 

Refrigerator 

Freezer 

Refrigerator 
Refrigerator 
Freezer 

Refrigerator 

Refrigerator 

Refrigerator 

Freezer 

Refrigerator 



1-2 days 
9 months 

3- 4 days 

4- 6 months 

1-2 days 
6-8 months 
1-2 days 

4 months 
1-2 days 
9 months 
3 days 

2 months 

1- 2 days 
3-4 months 

3- 5 days 
6-9 months 

4- 6 months 

3- 5 days 
6-12 months 

4- 6 months 
6-9 months 
3-5 days 
3-4 days 

2- 3 months 

2 weeks 

3- 5 days 
1-2 months 

3 weeks 
1 week 

5 days 

1 month 

2 months 



food poisoning 107 



can contain the bacteria, so always cook eggs 
thoroughly to kill the salmonella. 

• Store eggs in their cartons in the coldest part of 
the refrigerator, never on the refrigerator door, 
to prevent multiplication of bacteria. 

• Generally, throw out any food that has mold 
(except cheese, which can be consumed safely 
once the mold has been removed). 



• Use a microwave that has a turntable because 
microwaves heat food unevenly. 

• Do not season wooden salad bowls with oil 
because the oil can become rancid. 

• Thoroughly clean the sink after working with 
meat and poultry. Clean the sink and counters 
with detergent that contains bleach, which kills 
bacteria. 



SYMPTOMS OF FOOD POISONING 



If you have 


It could be 


Ulcer pain, abdominal pain, fever, nausea, vomiting, and diarrhea one week 


Anisakiasis 


after poisoning 




Explosive watery diarrhea, abdominal cramps, dehydration from a few hours to 


Asiatic cholera 


a few days after ingesting the bacteria 




Gastroenteritis, diarrhea, nausea/vomiting appearing 1—6 hours after eating 


Bdcillus cefeus 


Slurred speech, double vision, muscle paralysis 4—36 hours after meal 


Botulism 


Cramps, fever, diarrhea, nausea/vomiting appearing 1-5 days after eating and 


Campy lobacteriosis 


lasting up to 1 0 days 




Nausea, vomiting, and diarrhea within 6-12 hours after eating, followed by 


Ciguatera 


low blood pressure and heart rate; severe itching, temperature reversal. 




numbness/tingling of extremities (may last months) 




Watery diarrhea, nausea/vomiting appearing within hours to a week after eat- 


Enteric E. coli 


ing (severe cases include blood in diarrhea; enterhemorrhagic infection 




includes bloody diarrhea and kidney failure) 




Mild abdominal pain and diarrhea, nausea/vomiting 6—16 hours after eating 


Food poisoning 


Explosive diarrhea, foul-smelling, greasy feces, stomach pain, gas, appetite 


Giardiasis 


loss, nausea/vomiting within 1-2 weeks 




Fever, headache, diarrhea, meningitis, conjunctivitis, miscarriage appearing 


Listeriosis 


within days to weeks after ingestion 




Burning mouth/extremities, nausea, vomiting, and diarrhea within a few hours 


Neurotoxic shellfish poisoning 


Burning mouth/extremities, nausea/vomiting, diarrhea, muscle weakness, paral- 


Paralytic shellfish poisoning 


ysis, breathing problems within a few minutes 


Diarrhea, rumbling bowels, fever, vomiting, cramps 6-72 hours after eating 


Salmonellosis 


Itching, flushing cramps, diarrhea, nausea/vomiting, burning throat (severe 


Scombroid poisoning 


infection includes low blood pressure and breathing problems) within a few 


minutes to hours 




Gastroenteritis, diarrhea, nausea/vomiting 1-7 days after eating 


Shigellosis 


Explosive diarrhea, cramps, vomiting not longer than a day between 30 min- 


Staphylococcal food poisoning 


utes-5 hours after eating 


Diarrhea, nausea/vomiting, fever followed by muscle pain and stiffness 2-3 


Trichinosis 


weeks later 




Gastroenteritis, explosive diarrhea, nausea/vomiting, cramps 8-30 hours after 


Vibrio food poisoning (V. paraliaemo- 


eating (V. vulnificus can lead to fatal blood infection) 


lyticus, V. vulnificus) 



108 formaldehyde 



• Sponges used to clean the sink, dishes, and/or 
countertops should be decontaminated by micro- 
waving them or putting them in the dishwasher. 
Both methods remove virtually 100 percent of 
bacteria, mold, and yeasts. 

Treatment (general) 

In all cases of food poisoning, symptoms should be 
treated much like a bout of flu, including drink- 
ing fluids (water, tea, boufllon, and ginger ale) 
to replace fluid loss. Mfld cases may be treated at 
home, with a soft diet, including some salt and 
sugar. Most cases of food poisoning are not serious 
(except for botulism) and recovery usuaUy occurs 
within three days. Samples of any food left from 
recent meals should be saved for testing if possible. 

The greater danger from food poisoning is not 
the toxin itself but the body's natural response to 
poison — vomiting and diarrhea — which robs the 
body of vital fluids. If dehydration becomes seri- 
ous, food poisoning victims need to be hospitahzed 
and given fluids intravenously. However, poisoning 
from E. coli bacteria can lead to severe enterhem- 
orrhagic infection, which can include bloody diar- 
rhea, leading to kidney failure. One of the most 
recent E. coli scares occurred in September 2007, 
when the CDC announced that at least 28 people 
in eight states had become ill after consuming ham- 
burger meat tainted with E. coli. 

Although the time between ingestion and onset 
of symptoms varies according to the cause of poi- 
soning, symptoms usually develop within one to 
six hours for some types of shellfish poisoning, 
between one and 12 hours for bacterial toxins, and 
between 12 and 48 hours for viral and salmonella 
infections. Symptoms also vary depending on how 
badly the food was contaminated, but there will 
often be nausea and vomiting, diarrhea, stomach 
pain, and — in severe cases — shock and collapse. 

A doctor should be called if severe vomiting or 
diarrhea appears suddenly, if the victim collapses 
or if there is a suspicion of food poisoning and the 
victim is a child, an elderly person, or someone with a 
chronic illness. 

Symptoms 

Typical symptoms of food poisoning and their possi- 
ble causes are provided in the table presented here. 



Reporting food poisoning 
According to the U.S. Department of Agriculture's 
Safety and Inspection Service, consumers should 
report possible food poisoning if the food was eaten 
at a large gathering: if the food was from a restau- 
rant, deli, sidewalk vendor, or other kitchen that 
serves more than a few people; or if the food is a 
commercial product (such as canned goods or fro- 
zen food), since contaminants may have affected 
an entire lot or batch. 

When making a report, officials need to know: 

• Your name, address, telephone number 

• Detailed explanation of the situation that leads 
you to believe this is a case of food poisoning 

• When and where the suspected food was 
consumed 

• Who ate it 

• Name and address of where the food was 
obtained and/or consumed 

• If the food is a commercial product, the manu- 
facturer's name and address and the product's lot 
or batch number 

• If the tainted food is meat or poultry, the USDA 
inspection stamp on the wrapper identifies the 
plant where the food was made or packaged 

formaldehyde This colorless, pungent irritant gas 
has an unpleasant odor and is considered to be 
supertoxic. It is most commonly found as formalin, 
a solution of 40 percent formaldehyde, water, and 
methanol used in medicine to preserve tissue speci- 
mens. It is also found in many everyday products: 
the glue and resin odor in new automobiles and 
furniture is formaldehyde; it is also contained in 
antiseptics, disinfectants, fabric sizing, some explo- 
sives, and adhesives. The higher the concentration 
of formaldehyde in a product, the greater the dan- 
ger of explosion. 

Formaldehyde is the most common chemical 
irritant in modern buildings — found in plywood, 
particleboard, stain-resistant carpets, insulation, 
and adhesives in flooring. However, the amount 
of formaldehyde emitted by these products fades 
in time. Workers and homeowners are exposed to 



foxglove 109 



low levels of formaldehyde from cloth, foam insu- 
lation, and plywood (especially in mobile homes). 
Formaldehyde has been classified as a human car- 
cinogen by the International Agency for Research 
on Cancer and as a probable human carcinogen by 
the U.S. Environmental Protection Agency. 

Symptoms 

Most dangerous when inhaled or ingested, form- 
aldehyde is less toxic when absorbed through 
the skin. It attacks the respiratory system, and, 
if it is ingested, victims experience immediate 
severe abdominal pain, with vomiting, pain in the 
throat and diarrhea, corrosive gastritis and collapse 
within a few minutes, loss of consciousness and 
liver failure, with death from circulatory failure. 
Shock may cause death within a few hours up to 
two days. If the patient does not die, recovery may 
be rapid. 

Inhalation of fumes irritates the eyes, nose, and 
respiratory tract; chronic inhalation causes pulmo- 
nary edema and death. Skin contact (especially 
with paper and cloth containing formaldehyde) 
causes discoloration and may result in sloughing 
and allergic dermatitis. 

Treatment 

Gastric lavage immediately after ingestion, fol- 
lowed by large amounts of water and then a saline 
cathartic. In the event of skin contamination, wash 
thoroughly. Otherwise, treatment is supportive; 
dialysis may be effective. 

formalin See formaldehyde. 



foxglove (Digitalis) [Other names: dead man's thim- 
bles, fairy bells, fairy cap, fairy finger, fairy glove, 
fairy thimbles, folks gloves, foxes glofa.] Named 
for the resemblance of its flowers to fingers of the 
fairy "folks gloves," the foxglove has been consid- 
ered medically useful since the first century a.d. 
and was first written about as a drug in the year 
1200. The name refers to any of about 30 species 
of plants including the common foxglove (D. pur- 
purea), which is a powerful poison and plant source 
of the heart drug digitalis. 



Together with paintbrush, speedwell, snap- 
dragon, and monkeyflower, foxglove is a biennial 
member of the figwort family (Scrophulariaceae). 
During its first year, the plant produces a soft 
rosette of full, tapering, finely toothed leaves cov- 
ered with white down, and on the second year it 
produces a beautiful, tall fiower stalk column of 
three to five feet, with bell-shaped hanging flowers 
of yellow, white, pink, and purple. The stalk has a 
few small leaves and a long succession of flowers 
that open from the bottom to the top; each flower 
droops over the one below it on the stalk, and the 
flowers bloom in midsummer. 

Native to Europe, the Mediterranean region, 
and the Canary Islands, foxglove is grown as an 
ornamental in the United States and is often seen 
in foundation plantings of older homes. It is also 
naturalized on the Pacific coast from northern Cali- 
fornia to British Columbia. 

Its name originates in Britain, where residents 
called it "folks gloves" (the gloves of the little 
people, or fairies) and befieved that the small spots 
on the lower lip of the foxglove flower were tiny 
fairy fingerprints. It was also called "dead man's 
thimbles" because of its shape and toxicity, and its 
Latin genus — Digitalis — also refers to a finger, or 
thimble. 

In fact, it was in Britain that its usefulness as 
a heart medication was first discovered in 1775, 
when the physician to Benjamin Franklin discov- 
ered that a cold infusion made from the dried, 
powdered leaf of the foxglove acts as a heart stimu- 
lant and also a diuretic. The strengthened heart 
pumps more blood through the kidneys, carrying 
off water that has accumulated in the tissues. 

Foxglove is considered by some to be a magical 
plant, ruled by the planet Venus, and has, since 
ancient times, been considered to be an herb of 
protection. Welsh housewives rubbed foxglove 
leaves into the stone cracks in their floors and 
painted crossed lines on the floor with foxglove dye 
to prevent evil from entering their homes. 

Digitalis works by slowing the heartbeat and 
making it stronger, thereby increasing the efficiency 
of the heart. It reduces congestion in the veins and 
causes the kidneys to produce more urine. In the 
past, digitafis was administered by using the entire 
leaf, until digitoxin was isolated in 1869. Digoxin 



110 fugu 



was isolated in 1930, which allowed physicians to 
refine the dosage and control the drug's action on 
the heart. No synthetic drug has been discovered 
that can take the place of Digitalis purpurea. 

Recent research also suggests digitalis may be 
beneficial against glaucoma and as a component 
in a drug program in the treatment of muscular 
dystrophy. 

Poisonous part 

All parts of this plant — particularly the leaves — are 
poisonous and contain several glycosides that affect 
the heart and kidneys as well as irritant saponins. 
Ingestion of the dried or fresh leaves, which are not 
rendered harmless by cooking, will cause a severe 
case of poisoning. Most cases of foxglove poison- 
ing have resulted from therapeutic overdose or by 
drinking foxglove herbal teas, not from accidental 
ingestion. Children have been poisoned after suck- 
ing on flowers or swallowing the seeds. 

Symptoms 

Eating even small amounts of foxglove leaves, flow- 
ers, or other parts can dangerously disrupt heartbeat 
rhythm. In large amounts it can depress heart 
function or stop it completely. Symptoms appear 
within 20 to 30 minutes after ingestion and include 
nausea, vomiting, diarrhea, stomach pain, severe 
headache, blurred vision, loss of appetite, irregular 



heartbeat and pulse, delirium, tremors, convul- 
sions, and death from paralysis of the heart muscle. 
In excess amounts, foxglove increases the force of 
the heart's contractions to the point where it causes 
irritation and stimulates the central nervous system. 
Some sensitive individuals experience headache, 
rash, and nausea from handling the plant. 

Treatment 

Gastric lavage followed by the administration of 
activated charcoal, together with potassium chlo- 
ride every hour (unless urination stops). Victims 
must have their heart and potassium levels con- 
stantly monitored. 

See also digitalis; digitoxin; digoxin; glyco- 
sides; SAPONIN. 

fugu See pufferfish; tetrodotoxin. 

fungicide Fungicides are inorganic and organic 
compounds used to protect against rot and elimi- 
nate fungi. While some are fairly nontoxic to 
humans, others are extremely poisonous. Among 
the most common substances used as fungicides 
are mercury and copper compounds, pentachlo- 
rophenol, dithiocarbamates, tetramethylthiuram 
disulfide, hexachlorobenzene, and iodine. 



G 



galerina mushroom (Cortinarius speciosissimus, C. 
gentilis, Galerina venenata, G. autumnalis and C. 
orellanus) Members of the Cortinarius genus, they 
cause some of the same symptoms. The brown- 
capped galerinas are also known as deadly cort, 
deadly galerina, and deadly lawn galerina; all are 
supertoxic. 

C. orellanus is found primarily in Europe; C. gen- 
tilis, G. venenata, G. autumnalis (deadly galerina) and 
C. speciosissimus are found throughout the United 
States, particularly in the Northeast. 

Poisonous part 

The poison orellanin found in these mushrooms 
is toxic to the kidneys, but experts beheve the 
mushrooms contain other as-yet-unidentified 
poisons. 

Symptoms 

Latency period following ingestion is longer than 
10 hours and may last as long as two weeks; 
when symptoms appear, they include acute stom- 
ach pain, headaches, back or joint pain, kidney 
failure, damage to the intestines, genital organs, 
liver, heart, and nervous system. The victim's 
course may seem to improve, only to worsen and 
improve again until death finally occurs several 
months later. 

Treatment 

There is no antidote or successful treatment known. 
Vomiting soon after ingestion may expel the poison, 
and medical treatment may save some victims. 

See also cortinarius mushrooms; mushroom 
poisoning; mushroom toxins. 

gasoline See petroleum distillates. 



gelsemine A plant alkaloid found in yellow jes- 
samine, gelsemine depresses and eventually para- 
lyzes motor nerve endings, with contractions or 
spasms and — in severe cases — convulsions and 
respiratory arrest. 

See also alkaloids; jessamine, yellow. 

gelsemium (Gelsemium sempervirens) [Other 
names: Carolina Jasmine, yellow jasmine, 
sariyasemin.] This flowering climbing vine 
belongs to the family Loganiaceae and grows in 
the piedmont and coastal areas of the southeastern 
United States. Its flowers are funnel shaped and 
have a strong fragrance. Historically the roots and 
rhizome of the gelsemium were used to treat neu- 
ralgia and migraine. 

The woody stem of gelsemium contains a milky 
juice and bears shiny lanceolate leaves and axil- 
lary clusters of one to five flowers, which bloom in 
early spring. The fruit is composed of two jointed 
pods that contain many flat-winged seeds. 

Gelsemium sempervirens contains a long list of 
ergot type alkaloids, including gelsemicine, which 
is a central nervous system depressant and convul- 
sant; and gelsemine, which has analgesic, hypoten- 
sive, cardiodepressant, and central nervous system 
depressant properties. In 2006, Chinese researchers 
announced that they had isolated three new alka- 
loids and a new extract artifact, gelsebamine, from 
gelsemium. The gelsebamine was found to inhibit a 
specific human lung adenocarcinoma cell line. 

Use of gelsemium for treating various ailments 
in cats has been reported anecdotally, while use in 
humans is most widespread in Mexico, where it 
has been given for asthma, dysmenorrhea, gonor- 
rhea, hypertension, malaria, and rheumatism. The 
fresh root is used to make a homeopathic remedy. 



Ill 



112 GHB 



Poisonous part 

All parts of the plant are poisonous, including the 
nectar and the flowers. The most toxic compounds 
are gelsemine and gelseminine, which depress the 
motor nerves. The toxic and therapeutic doses of 
gelsemium are very close. Eating just one flower 
has reportedly been deadly for children. It is possi- 
ble to absorb the toxins through the skin, especially 
if there are cuts, abrasions, or it has been otherwise 
compromised. 

Symptoms 

Symptoms typically begin within 30 minutes of 
ingestion but may start immediately. These include 
difficulty in the use of voluntary muscles, muscle 
rigidity and weakness, dizziness, dry mouth, visual 
disturbances, trembling of the extremities, profuse 
sweating, respiratory depression, convulsions, and 
loss of speech. With large doses, paralysis, feeble 
respiration, and death from respiratory failure can 
occur. Death may occur within one to seven and 
one-half hours from ingestion. 

Treatment 

Prompt evacuation of the stomach by an emetic if 
the patient's condition allows. Equally important is 
artificial respiration, aided by early subcutaneous 
administration of ammonia, strychnine, atropine, 
or digitalis. 

GHB (gamma-hydroxybutyric acid) [street names: 
"G," goop, scoop, liquid x, liquid ecstasy, caps, 
grievous bodily harm] Initially used by body 
builders to stimulate muscle growth, GHB has 
become a popular recreational drug used by ado- 
lescents and young adults, especially during parties 
and raves, because it induces relaxation and a high 
that can last up to four hours. GHB can be made 
from ingredients such as gamma -butyrolactone, 
a solvent used as a paint stripper, or butanediol, 
which is used in the production of plastics and 
adhesives. The drug is available as a powder, tablet, 
capsule, and clear liquid. 

Because GHB is odorless, colorless, and virtually 
tasteless (it is slightly salty), it can be slipped into 
drinks without detection, and so it has become a 
popular date rape drug, along with ecstasy. The 



drug was banned by the Food and Drug Adminis- 
tration in 1990 after 57 people sought emergency 
treatment at poison control centers and emergency 
rooms for serious to life-threatening symptoms. 
Since that time GHB has been associated with sev- 
eral deaths and has been categorized as a Schedule 
I drug according to the Controlled Substances 
Act. However, a form of GHB — sodium oxybate, 
Xyrem — was approved by the FDA on July 17, 
2002, for treatment of a rare form of narcolepsy. It 
is available only by prescription and is tightly regu- 
lated. Most of the GHB used in the United States is 
manufactured illegally in the States. 

Symptoms 

The effects of GHB can be felt within five to 20 min- 
utes of taking the drug and the high can last up to 
four hours. At lower doses, GHB relieves anxiety and 
produces relaxation. When it is combined with other 
drugs such as alcohol it can cause nausea, breathing 
difficulties, and loss of muscle control. Withdrawal 
effects include insomnia, tremors, sweating, and 
anxiety. At higher doses, users may encounter diffi- 
culty thinking, hallucinations, slurred speech, head- 
ache, amnesia, coma, or death. 

Treatment 

Because absorption and onset of symptoms are 
so rapid after ingestion, washing out the stomach 
typically has little impact. Thus treatment for GHB 
poisoning is largely supportive. Activated charcoal 
can be tried. There is no known antidote to GHB. 

giant milkweed (Calotropis procera, C. gigantea) 

This tree is found in the tropical Americas and 
Africa; its sap is used as an arrow poison in Africa. 
The treelike shrubs have rubbery leaves and clus- 
ters of white or lilac flowers with a sweet scent. 
The seeds have silky attachments, similar to other 
types of milkweed seeds, which are shaken from 
the pods as they dry. The two species are different 
heights (C. procera is less than six feet; C. gigantea 
may grow to 15 feet). 

Poisonous part 

The latex sap contains a mixture of cardiac gly- 
cosides with digitalis-like action, and unidentified 
allergens. 



Gila monster 113 



Symptoms 

Ingestion results in irritation, burning, and swelling 
of the mucous membranes, but because of the bad 
taste ingestion of large amounts is not normally a 
problem. In addition, skin contact may cause an 
allergic reaction. Exposure to the eyes (cornea) 
may cause a severe keratoconjunctivitis. 

Treatment 

The ingestion of a large amount of this plant may 
produce heart irregularities, which are managed by 
monitoring by electrocardiogram. 

See also cardiac glycosides; digitalis. 

giardiasis An infection of the small intestine caused 
by the protozoan Giardia lamblia, which is found in 
the intestinal tract and feces. Contamination occurs 
when sewage is used as a fertilizer or when food han- 
dlers don't wash their hands. Although giardiasis is 
generally found commonly in tropical countries and 
travelers to those areas, in recent years outbreaks 
have been common in the United States among peo- 
ple in institutions, preschool children, and in catered 
affairs and large public picnic areas. It is most com- 
mon in this country where large numbers of young 
children gather. It is spread by contaminated food or 
water or by direct personal hand-to-mouth contact. 
Infection can be prevented by thoroughly washing 
hands before handling food. 

Symptoms 

Giardiasis is not fatal and will eventually pass, 
and about two-thirds of infected people have no 
symptoms. When they do occur, symptoms appear 
about one to three days after infection and are 
uncomfortable. They include explosive diarrhea, 
foul-smelling and greasy feces, stomach pains, gas, 
loss of appetite, nausea, and vomiting. In some 
cases, the infection can become chronic. Giardiasis 
is diagnosed by examining a fecal sample for the 
presence of the parasites. 

Treatment 

Acute giardiasis usually runs its course and then 
clears up, but antibiotic metronidazole or quina- 
crine will help relieve symptoms and prevent the 
spread of infection. 



Gila monster (Heloderma suspectum) The Gila 
monster is one of only two poisonous lizards in the 
world; both are similar in appearance and habits. 
This sluggish, shy little fellow grows to about 20 
inches, with a stout body, black and pink spots, 
and bands extending onto a blunt tail and beadlike 
scales. It has a black face, with large toes and strong 
claws, and is smaller than its poisonous relative, 
the Mexican beaded lizard. 

Named after the Gila River basin, the Gila mon- 
ster lives in the gravelly and sandy soils found in 
the deserts of the Southwest, particularly in Ari- 
zona, southern Utah, and New Mexico. It prefers 
rocks and other animals' burrows; it may also dig 
its own holes. Gila monsters mate during summer 
and lay between three and five eggs in autumn and 
winter, and more than 95 percent of their time is 
spent underground. 

Poisonous part 

The venom of this lizard, used principally to immo- 
bilize prey, is extremely dangerous for humans as 
well. It is produced in eight glands in the lower 
jaw; venom is secreted into the mouth and then 
flows through the grooves of the teeth into the 
bite wound as the lizard chews; it is not injected as 
is snake venom. The whole system is not particu- 
larly efficient, requiring the Gila monster to hang 
on to its prey for some time and chew its tissues, 
enabling the poison to flow. The bite is extremely 
painful but rarely fatal (no deaths have been 
reported in modern times), but the Gila monster 
is extremely tenacious; often the victim must be 
cut away. 

Symptoms 

Severe pain at the wound site, swelling, weakness, 
tinnitus (ringing in the ears), nausea, breathing 
problems, cardiac failure, and sometimes death are 
symptoms that occur within one to three hours 
after the bite; their severity depends on the amount 
of venom injected, where the wound is located, 
and the victim's health. 

Treatment 

There is no known antivenin. Treatment is sup- 
portive, with tetanus prophylaxis and pain relief. 
See also Mexican beaded lizard. 



114 glue 



glue See solvent abuse. 

glycoside Also known as glucosides, the gly- 
cosides are more common in the plant kingdom 
than alkaloids. Glycosides are a group of com- 
pounds containing at least one type of sugar that 
are released when the plant is eaten. (Glyco comes 
from the root word meaning "sugar.") The amount 
of glycoside in a plant depends on genetics, the 
part of the plant, its age and, to a large degree, 
environmental factors such as climate, moisture 
supply, and fertility of the soil. While many gly- 
cosides are not poisonous, a number of them are, 
including cardiac glycosides, cyanogenic glycosides, 
and saponins. 

Glycosides that yield hydrocyanic acid after 
hydrolysis are called cyanogenetic; one of the 
most common is the glycoside amygdalin, found in 
many members of Rosaceae plants that have cya- 
nogenetic compounds, including hydrangea, flax, 
cassava, hma bean, cherry, apple, white clover, and 
vetch seed. 

See also alkaloids; cardiac glycosides; cyano- 
genic glycosides; saponin. 



golden dewdrop (Duranta repens L.) [Other names: 
pigeon berry, sky-flower.] This large shrub usually 
cultivated as a hedge is native to Key West and 
is also found in southern Texas, the West Indies, 
Hawaii, Guam, and Australia. It produces small, 
light blue or white flowers and masses of poisonous 
orange berries. 

Poisonous part 

The berry contains toxic saponins, but reports of poi- 
soning with them have occurred only in Australia. 

Symptoms 

Sleepiness, fever, tachycardia, swelling of the lips and 
eyelids, convulsions, and gastrointestinal irritation. 

Treatment 

Gastric lavage, control of convulsions with diaz- 
epam and maintenance of fluid and electrolyte 
balance. 

See also saponin. 



gout stalk (Jatropha podagrica) This plant is a 
member of a large genus of shrubs or small trees 
with a three-sided seed capsule, found throughout 
the Western Hemisphere. 

Poisonous part 

The seeds are poisonous and contain jatrophin 
(curcin), a plant lectin (toxalbumin), and cathartic 
oils. Ingestion of just one seed can be serious. The 
plant lectin inhibits protein synthesis in cells of 
the intestinal wall and may cause serious or fatal 
poisoning. 

Symptoms 

The onset of symptoms (nausea, vomiting, and 
diarrhea) occurs rapidly, unlike poisoning with 
other plants with toxic lectins. 

Treatment 

Treat symptoms; give fluids. 

ground cherry (Physalis) There are about 17 
species of this plant growing in the United States, 
most with an attractive fruit resembling a Chinese 
lantern; inside the papery pod is a berry filled with 
tiny seeds. 

Poisonous part 

The unripe berries are poisonous and contain toxic 
solanine glycoalkaloids. 

Symptoms 

While solanine rarely is toxic to adults, children 
can be fatally poisoned. Symptoms include stom- 
ach irritation, a harsh, scratchy feeling in the 
throat, diarrhea, and fever. 

Treatment 

Replace fluids, treat symptoms, and give supportive 
care. 

grouper, spotted Any of a number of species of 
fish in the family Serranidae (including yellowfin) 
widely found in warm seas with large mouths 
and heavy bodies; they can grow to be more than 
six feet long. Many carry a toxic substance in the 



Gyromitra 115 



flesh that can cause a type of food poisoning called 
ciguatera. 

Poisonous part 

The toxin believed to be involved in ciguatera is fat 
soluble, odorless and tasteless, and is not destroyed 
by heat. 

Symptoms 

After eating, symptoms may develop quickly or 
slowly and involve tingling sensations in the lips 
and mouth followed by numbness, nausea, vomit- 
ing, abdominal cramps, weakness, paralysis, con- 
vulsions, skin rash, coma, and death in about 12 
percent of cases. 

Treatment 

Recent research suggests that prahdoxime chlo- 
ride (a chohnesterase reactivator) is an effective 
antidote. 

See also ciguatera; fish contamination. 

grouper, yellowfin See grouper, spotted. 

Gyromitra This genus of mushroom, also known 
as the false morel, contains a toxin usually removed 
during cooking, although a few individuals are 
sensitive to it even when the mushroom is cooked 
completely. The species has no gills, and its spores 
develop in microscopic sacs on the surfaces of the 



fruiting bodies. The appearance of the body of the 
fungus gives this mushroom its nickname, brain 
fungi. While many species of Gyromitra are edible, 
it usually takes an expert to tell the difference. 

Poisonous part 

While the chemical ingredient in this species is not 
known, many varieties contain gyromitrin, which 
is hydrolyzed to form the active toxin monometh- 
ylhydrazine, a substance that affects the central 
nervous system and is also used as rocket fuel. 
This toxin is volatile and dissolves readily in water; 
therefore, the mushroom may be made edible 
by air drying or extracting the toxin with boiling 
water. 

Symptoms 

Between six and 24 hours after ingestion or 
inhalation of the vapor while cooking, symptoms 
suddenly appear: The victim begins to vomit and 
develops dizziness, fatigue, and muscle cramps. 
In severe cases, this may be followed by delirium, 
coma, and convulsions and can sometimes be fatal. 
In nonfatal cases, victims recover within two to 
six days. 

Treatment 

Supportive, which may include blood transfusions 
and correction of acidosis. Intravenous pyridoxine 
is the specific antidote. 

See also monomethylhydrazine; mushroom poi- 
soning; MUSHROOM TOXINS. 



habu, Okinawa (Trimeresurus flavoviridis) The 

most dangerous pit viper in Asia, this large, aggres- 
sive snake, known as one of the collective group 
called fer-de-lance, is found on the Amami and 
Okinawa groups in the Ryukyu Islands — often in 
houses. Marked with a wavy band of dark green 
splotches, it sometimes grows to be five feet long 
and can cause disability or death. Its smaller rela- 
tive, the kufah (Trimeresurus okinavesis), is also dan- 
gerous. Both are happy to live in trees, along with 
the other genus of this group, Agkistrodon. 

Symptoms 

Because the venom interferes with the coagula- 
tion of the blood, it hemorrhages into muscles 
and the nervous system and results in bleeding 
from the gums, nose, mouth, and rectum. Shock 
and respiratory distress is followed by death if 
untreated. 

Treatment 

Antivenin is available. 

See also antivenin; fer-de-lance; pit vipers; 

SNAKES, poisonous. 

Halcion See benzodiazepines; sleeping pills. 
Haldol See antipsychotic/psychometric drugs. 



liculosa, P. cyanescens, P. baeocystis, P. cubensis), cono- 
cybes (Conocybe cyanopus, C. smithii), and stropharias, 
all of which produce visual and auditory hallucina- 
tions about 1 5 minutes after eating. 

The Conocybe and Psilocybe mushrooms contain 
psilocybin and psilocin as active constituents. 

Symptoms 

The onset of effects for all varieties usually occurs 
within three hours of ingestion, and symptoms 
include drowsiness, loss of ability to concentrate, 
dizziness, and sometimes muscle weakness. The 
hallucinogenic effects are dose dependent and 
may vary according to the personality of the per- 
son; both space and time distortion are reported, 
together with visual and auditory imagery. The hal- 
lucinations are usually described as pleasant. 

Treatment 

Recovery following ingestion of such a mushroom 
is normally uneventful. The period of intoxication 
is not long, usually between three and six hours, 
after which all symptoms disappear. However, 
there is a danger that patients may become destruc- 
tive during the hallucinatory period, and therefore 
their movements should be restricted. Phenothi- 
azine drugs may be used to end the psychosis if 
extreme agitation is experienced. 

See also Mexican hallucinogenic mushroom; 
mushroom poisoning. 



hallucinogenic mushrooms A group of mush- 
rooms, important to the sacred ceremonies of 
the American Indian religions (and also to drug 
abusers), that produce hallucinations when eaten. 
These mushrooms include three main groups: the 
psilocybes (Psilocybe caerulescens, P. mexicana, P. pel- 



harlequin snake See coral snake, eastern. 

Helicobacter pylori This bacterium is believed to 
cause most stomach ulcers and almost all duode- 
nal ulcers, and is believed to exist in groundwater 



116 



hemlock, poison 117 



throughout the United States. In 1983, the bacte- 
rium was first found in the stomach tissue of ulcer 
patients. While half the world's populations are 
believed to be infected (including an estimated 40 
million Americans), it only causes ulcers in 10 to 
20 percent of its hosts. Still, one out of every 10 
Americans has an ulcer, and H. pylori is implicated 
in 90 percent of those cases. 

Symptoms 

Nausea and stomach pain, vomiting and fever last- 
ing between three and 14 days. Virtually every- 
one with the bacteria has chronic gastritis (a mild 
inflammation of the stomach lining), which may 
last for decades. Some people with the infection 
don't have ulcers but have nausea, gas, bloating, 
and burning stomach pain. 

Diagnosis 

Blood tests can determine the presence of antibod- 
ies to the bacteria, which can tell if you have ever 
had the infection but not if it's active. A biopsy can 
reveal H. pylori. Breath tests are currently being 
studied and may be available in the near future. 

Treatment 

About 90 percent of H. pylori infections can be 
cured with a combination of anti-ulcer medication 
and specific antibiotics. However, the treatment is 
not easy; it involves taking 12 to 16 pills a day for 
two weeks and carries the risk of some side effects, 
such as fatigue and dizziness. Because the treat- 
ment may not be completely successful, follow-up 
testing at least four weeks after completing treat- 
ment may be needed to make sure the bacteria are 
no longer present. If tests reveal no bacteria, the 
patient is not likely to be reinfected ever again. Per- 
sistent infection may require a different medication 
for longer period of time. 

Complications 

The organism has also been found in a dispropor- 
tionately large number of patients with certain 
kinds of stomach cancer. Some scientists suggest 
the infection may triple the risk of this rare cancer. 
While there appears to be a relationship between 
the bacteria and stomach cancer, these cancers are 
becoming less common in the United States, and 



therapy for H. pylori has not been recommended as 
a preventive measure. 

Prevention 

Chlorine in pubhc drinking water kills the bacteria, 
but shallow wells may be contaminated by surface 
water tainted with the bacterium (deeper wells are 
less likely to have the bacterium). Normal water 
testing procedures can't identify the presence of 
H. pylori, and there is no test at present that you 
can use to test your well. However, private water- 
testing labs can test water for microscopic particu- 
lates, which will determine if the well water has 
been contaminated with surface water and thus, 
by bacteria. You can install an ultraviolet disinfec- 
tion system to treat contaminated water. Charcoal- 
based tap filters may not be a good choice, because 
bacteria can form on the charcoal. 

hemlock, deadly See hemlock, poison. 

hemlock, ground See yew. 

hemlock, lesser See hemlock, poison. 

hemlock, poison (Conium maculatum) [Other 
names: California fern, deadly hemlock, herb bon- 
nett, kill cow, lesser hemlock, muskrat weed bunk, 
Nebraska fern, poison parsley, poison root, snake 
weed, spotted hemlock, spotted parsley, wode 
whistle.] The ancient poison drink of Socrates, 
poison hemlock is rapidly fatal. The plant (which 
resembles a carrot) has large lacy leaves as much as 
four feet long that produce a disagreeable garhcky 
odor when crushed, and a white root. It is found 
in South America, northern Africa and Asia, and 
in the United States and Canada where it has been 
naturalized. In Europe, it is called "fool's parsley." 

Poisonous part 

Leaves are most toxic when the plant is flowering, but 
all parts of the hemlock are deadly. Its root resembles 
the wild carrot, and its seeds have been mistaken for 
anise. Hemlock contains coniine, a muscle relaxant 



118 hemlock, water 



similar to curare, and related alkaloids. In addition, 
quail may eat poison hemlock seeds and pass on 
the poison to a human who consumes the flesh. 
This type of secondary hemlock poisoning can cause 
diarrhea, vomiting, and paralysis in humans within 
three hours of eating the affected quail. 

Symptoms 

Responsible for many human fatalities, hemlock poi- 
soning can begin within 30 minutes after ingestion. 
Symptoms include gradual muscular weakness and 
increasing muscular pain, paralysis, blindness, respi- 
ratory problems, and death within several hours, 
which comes from paralysis of the lungs. 

Treatment 

Gastric lavage must be performed immediately 
after ingestion of the poison or it is ineffective; give 
diazepam to relieve convulsions. 
See also alkaloids; coniine. 



hemlock, water (Cicuta maculata, C. californica, C. 
douglasii, C. vagans, C. bolanderi, C. bulbifera, C. 
curtissii, C. occidentalis) One of the most poison- 
ous plants and the most violent poison contained 
in plants in the United States, the several species of 
water hemlock are found in waste places, pastures, 
and swamps of the northern temperate regions. 
Water hemlock is a perennial herb and member 
of the carrot family, growing up to eight feet tall 
with purple spots and small, white, heavily scented 
flowers. Underground, there is a bundle of roots 
that, when cut, smell very much like parsnips. 
Water hemlock (C. maculata) is found in eastern 
North America to the Great Plains; Cahfornia water 
hemlock (C. californica, C. bolanderi) in midwestern 
California; Douglas water hemlock (C. douglasii) 
along the Pacific coast and British Columbia; 
tuber water hemlock or Oregon water hemlock 
(C. vagans) in the Pacific Northwest; western water 
hemlock (C. occidentalis) in the Rocky Mountain 
states to the Pacific coast; bulbous water hemlock 
(C. bulbifera) in the northern United States. 

Poisonous part 

The entire water hemlock contains the poison 
cicutoxin, although the root has the most. Many 



people have been poisoned by mistaking water 
hemlock for parsnips or artichokes, and children 
have been poisoned by using water hemlock to 
make peashooters and whistles. One mouthful of 
the root may kill an adult, and many Americans 
(especially children) have died after eating this 
plant; 30 percent of water hemlock poisonings 
are fatal. The powerful nerve toxin causes excru- 
ciating spasms and convulsions so powerful that 
people have been known to bite through their own 
tongue and break their teeth. 

Symptoms 

This is a fairly fast acting toxic plant, with symp- 
toms beginning 15 minutes after ingestion, includ- 
ing restlessness, abdominal pain, nausea, vomiting, 
diarrhea, respiratory problems, hypersalivation, 
weak and rapid pulse, delirium, violent convul- 
sions, and — within one hour — death. 

Treatment 

Both emetics and cathartics are used to get the 
poison out of the body, and morphine and barbitu- 
rates can control convulsions. Once seizures appear 
imminent or have already occurred, gastric lavage 
should not be attempted without an anesthesiolo- 
gist. Prolonged problems in mental function and 
abnormal brain waves have been reported. 

henbane (Hyoscyamus niger) [Other names: black 
henbane, devil's eye, fetid nightshade, henbell, 
hog's bean, insane root, Jupiter's bean, poison 
tobacco, stinking nightshade.] This powerful 
plant is the most common species of the night- 
shade/potato family Solanaceae, comprising 11 
biennials or perennials. Naturahzed in the eastern 
United States, it is grown commercially in North 
America and is found wild in garbage dumps and in 
isolated spots in Great Britain, central and southern 
Europe, and western Asia. 

The annual form of the plant grows to one to 
two feet tall and then flowers and sets seed; the 
biennial produces only a tuft of basal leaves that 
disappear in winter leaving a root. In the spring, a 
branched flowering stem grows from this root that 
is usually much taller and more vigorous than the 
flowering stems of the annual plants. The whole 



hepatitis A 119 



henbane plant has a strong, unpleasant odor, and 
its leaves, if bruised when fresh, emit a strong 
narcotic smell similar to that of tobacco. Its root is 
a long, tapering brown tuber with a bad odor and 
could be mistaken for parsnips and eaten, with 
fatal results. 

Three drugs are made from the dried leaves of 
the henbane plant: Atropine, hyoscyamine, and 
scopolamine. In addition, the leaves are smoked as 
a narcotic and are prepared as a beverage in India. 

Poisonous part 

All parts of the plant are poisonous, especially 
the seeds, pods, and leaves, which contain vary- 
ing amounts of the belladonna alkaloids atropine, 
hyoscyamine, and scopolamine. The seeds have the 
highest amount of scopolamine, which depresses 
the central nervous system. 

Symptoms 

A fast-acting toxin (within 15 minutes), henbane 
produces symptoms similar to those caused by 
deadly nightshade or atropine poisoning. Children 
are poisoned by eating seeds and pods. Poison- 
ing causes dry mouth, tachycardia, fever, blurred 
vision, excitement, delirium, and confusion; hallu- 
cinations are frequently reported in children. 

Treatment 

If poisoning is severe, a slow intravenous admin- 
istration of physostigmine is given until symptoms 
subside. 



hepatitis A The hardy hepatitis A virus is the most 
common type of all the alphabet hepatitis viruses. 
It is spread by eating food or drinking water con- 
taminated with the virus. It then multiphes in the 
body and is passed in the feces. It can then be car- 
ried on an infected person's hand and spread by 
direct contact or by eating food or drink handled 
by that person. Unlike many other viruses, it can 
live for more than a month at room temperature 
on kitchen countertops, children's toys, and other 
surfaces, and it can be maintained indefinitely in 
frozen foods and ice. 

In 1992, 22,000 Americans were reported to 
have hepatitis A. Since 1996, however, with the 



introduction of a vaccine, the Centers for Disease 
Control and Prevention (CDC) has recommended 
vaccination for persons at increased risk. In 1999 
it was recommended that children who lived in 
1 1 states with the highest incidence of hepatitis A 
be vaccinated routinely, and that children in six 
additional states that had an incidence above the 
national average also be considered for vaccination. 
A study compared incidence rates in 2003 with 
those of the prevaccination period and found that 
rates declined 76 percent overall and 88 percent in 
the vaccinating states. Since 2001, rates in adults, 
especially men aged 25 to 39, have been higher 
than among children. 

Hepatitis A may be found in shellfish (especially 
oysters), raw or undercooked food, fruits and veg- 
etables, and well water contaminated by improp- 
erly treated sewage. Although there is no typical 
"season" for hepatitis A, it tends to occur in cycles. 
Mass foodborne contaminations have been found 
in frozen strawberries, imported lettuce, restaurant 
iced tea, raw oysters, and shellfish. 

Symptoms 

Incubation period of the virus ranges from 15 to 
50 days. A quarter of all people with hepatitis A 
won't have any symptoms; a few young children 
may have a low fever and achiness, but rarely 
jaundice. Children over age 12 may be much 
sicker, with fever (100-104°F), extreme tired- 
ness, weakness, nausea, stomach upset, pain in 
the upper right side of the stomach, and appetite 
loss. Within a few days, a yellowish tinge appears 
in the skin and whites of the eyes. Urine will be 
darker than usual, and the stool is light colored. 
Once the jaundice appears, patients begin to feel 
better. 

Diagnosis 

Blood tests showing antibodies to hepatitis A are 
the best diagnosis. Symptoms of hepatitis A are so 
similar to other diseases that a doctor needs test 
results to make the correct diagnosis. 

Treatment 

There is no drug treatment for hepatitis A. While 
symptoms appear, patients should rest and eat well- 
low-fat, high-carbohydrate, easily digested foods. 



120 herbicides 



such as crackers, noodles, rice, or soup, in small 
amounts are good choices. Antinausea medicine 
and acetaminophen can be prescribed. 

Complications 

Rarely, hepatitis A develops into fulminant hepati- 
tis in which the liver cells are completely destroyed. 
As the liver function stops, toxic substances build 
up and affect the brain, causing lethargy, confu- 
sion, combativeness, stupor, and coma. This can 
often lead to death, although the patient may live 
with aggressive treatment. If the victim does not 
die, the liver is able to regenerate and resume func- 
tion and the brain recovers. 

Prognosis 

Hepatitis A is less serious than other types of 
hepatitis viruses and causes only temporary liver 
damage, which is reversed as the body produces 
antibodies. Most people recover in a few weeks 
without any complications. However, it can occa- 
sionally be fatal; about 100 people die each year 
from this infection. 

Prevention 

To inactivate the virus, food must be heated at 
185°F for one minute. It is difficult to test water 
for hepatitis A, but treated municipal or county 
water supplies are safe. Patients are most infec- 
tious in the two weeks before symptoms develop. 
Food handlers who know they are infected should 
not work until they are past the infectious stages, 
which ends one week after first becoming jaun- 
diced. Even though federal regulations and post- 
ing of contaminated waters offer some protection, 
there is still a risk of contracting viruses when eat- 
ing raw shellfish. 

A new vaccine said to be 100 percent effective 
after a single dose became available in 1996. With 
earlier vaccines, more than 99 percent of people 
became immune after two doses; a booster is rec- 
ommended for this vaccine between six and 12 
months after the first dose. 

Those who aren't vaccinated who are exposed 
can prevent infection by getting a shot of immune 
globulin (pooled human blood plasma that con- 
tains protective antibodies against the disease). 
People who would need this shot include 



• all household members and sex partners of hepa- 
titis A patients, 

• close friends of infected schoolchildren, 

• food handlers whose co worker (s) gets the disease, 

• staff of prisons and institutions where at least 
two residents have hepatitis A. 



herbicides Chemicals used to kill weeds. They 
can be divided into two groups: those that are 
poisonous to anything with which they come in 
contact, including animals and humans in addition 
to weeds; and those that are poisonous only to a 
selected group of weeds and will not harm humans 
or animals. Contact weed killers commonly used 
include sodium chlorate, dinitrophenol derivatives, 
potassium cyanate, sodium arsenite, caustic acids 
and alkafis, petroleum distillates, trifluralin, diquat, 
and paraquat. 

See also Paraquat; petroleum distillates. 



herbs, unsafe Long before the beginnings of 
modern medicine, the earliest health care prac- 
titioners — the shamans, the medicine men, and 
the healers — prescribed herbs and herb extracts 
to treat disease. Many of these herbal medicines 
were beneficial (for example, digitalis heart 
drugs are extracted from foxglove). But many of 
the early remedies have been discovered to be 
quite dangerous — even toxic — inducing violent 
episodes of vomiting or seizures and causing 
serious liver, kidney, or other organ damage. 
Some cause abortions, and others are simply of 
no value at all. 

According to the Food and Drug Administra- 
tion, there are three categories of herbs: unsafe 
herbs, herbs of undefined safety for food use and 
safe herbs (GRAS — generally recognized as safe). 
For its own purposes, however, the FDA consid- 
ers herbs as foods, not as medicine. Still, the FDA 
notes that even the GRAS herbs can cause prob- 
lems if used to excess. "Too much of any herb is 
toxic," the FDA warns in one of its reports. In 
particular, eating too much red pepper, sorrel, or 
nutmeg can be decidedly toxic. 



hexachlorophene 121 



While plant ingestions are second only to drugs 
as the most common poisoning emergency in 
children, serious poisoning or death from ingest- 
ing herbs is rare because the amount of toxin is 
usually quite small. However, there has been an 
increase over the past 20 years in the public use 
of herbal remedies and traditional herbal healing 
products. 

In fact, brewing or mixing some herbal remedies 
can be dangerous, not only because of the toxic 
makeup of the plants, but because the content of 
various toxins varies considerably with the soil 
and chmate conditions in which the plant was 
grown. Beneficial and harmful components in any 
herb can vary tremendously from one garden to 
another, from one year to another, and even from 
one plant to another in the same garden grown at 
the same time. 

Unfortunately, in addition to natural toxicity 
in some plants, "herbal" or "traditional" prepara- 
tions may sometimes actually contain drugs such 
as phenyllbutazone, corticosteroids, salicylates, 
ephedrine, or toxic metal salts (mercury or lead). 

Herbal mail-order suppliers and health food 
stores do a brisk business in health food products, 
and there are almost 400 different herbs available 
in the form of commercial teas. But some teas con- 
tain plants that can be very dangerous — nutmeg, 
mandrake, or jimsonweed (identified as "thorn 
apple," its other name). There are also almost 200 
herbs blended into a variety of commercial ciga- 
rettes or smoking mixtures. 

See also comfrey; digitalis; foxglove; jimson- 
weed; MANDRAKE, AMERICAN; NUTMEG. 

heroin (diacetylmorphine) A narcotic drug derived 
from morphine, the principal alkaloid of opium, 
which is extracted from the pods of the opium 
poppy and often processed in Turkey. Currently, 
Afghanistan is the world's primary morphine/heroin 
source. 

Heroin was created in an attempt to find a 
safer type of morphine, and the resulting product 
was a would-be cough medicine called Heroin, 
named for the drug's presumably "heroic" ability 
to mimic the effects of morphine without causing 
addiction. Developers hoped the new drug would 



be used to cure morphine addiction. Unfortu- 
nately, heroin is in fact four times more addictive 
than morphine. 

Heroin is a white or brown powder (depend- 
ing on where it has been processed) that can be 
smoked, sniffed, or dissolved in water and injected. 
It can be smoked when the end of a cigarette is 
dipped in heroin powder and lighted (this is called 
ack-ack); "chasing the dragon" or "playing the 
organ" involves mixing heroin with barbiturates. 
The drug is lighted and the smoke inhaled. Subcu- 
taneous injection is called skin popping; intrave- 
nous injection is mainlining. 

In addition to its painkilling properties, heroin 
produces sensations of warmth, calmness, drowsi- 
ness, and a loss of concern for outside events. 
Long-term use causes tolerance, which means the 
user needs more and more of the drug to maintain 
the same level of intoxication. It also produces 
both psychological and physical addiction. Sudden 
withdrawal of the drug causes shivering, abdomi- 
nal cramps, diarrhea, vomiting, sleeplessness, and 
restlessness. 

As yet, there is no legal medical use for heroin 
in the United States, although a few researchers 
are investigating its ability to control cancer pain. 
Heroin is an accepted cancer painkiller in Britain; 
because it is stronger than morphine, it is a better 
and longer-lasting pain reliever. 

Symptoms 

Heroin is a central nervous system depressant. An 
overdose frequently results in death. Following an 
injection, the user feels an immediate rush; if an 
overdose, death occurs within a few minutes unless 
the drug was sniffed or injected under the skin 
(then death may take up to four hours). Symptoms 
include pinpoint pupils, slow and shallow breath- 
ing, vision problems, restlessness, cramps, cyanosis, 
weak pulse, low blood pressure, coma, and death 
from respiratory paralysis. 

Treatment 

The antidote is naloxone; treat symptoms. 
See also morphine; narcotics; opium. 

hexachlorophene See phenol. 



122 holly 



holly (Ilex) There are about 400 species of red- or 
black-berried plants, including the popular Christ- 
mas hollies, American holly (Ilex opaca), and Eng- 
lish holly (I. aquifolium). The hollies have alternate, 
glossy and thick-spined leaves (either single or 
clustered) with small, green flowers and bright red 
or black berries. Male and female flowers are usu- 
ally on separate plants. 

American holly is native from Massachusetts 
to Florida, west to Missouri and Texas; English 
holly is cultivated from Virginia to Texas, the 
Pacific Coast states, and British Columbia. Yau- 
pon (Ilex vomitoria), also known as Carolina tea 
and emetic holly, is native to the Atlantic and 
Gulf coast states and North Carolina to Texas and 
Arkansas. 

Poisonous part 

Berries (and in some reports, leaves) of this plant 
are poisonous and contain alkaloids, glycosides, 
saponins, terpenoids, caffeine, and theobromine (a 
caffeinelike alkaloid). In some species, the leaves 
are brewed for their caffeine and other xanthines. 

Symptoms 

In small doses, holly may be a nervous system 
stimulant. In large doses, it can cause nausea, 
vomiting, diarrhea, inflamed and numb sensations 
in the mouth, drowsiness, and altered state of con- 
sciousness. The berries are particularly poisonous 
and can be fatal to children if enough are eaten and 
the symptoms are not treated. Some estimate that 
20 berries are poisonous, but a fatal dose may be 
less in children. 

Treatment 

Administer fluids to prevent dehydration. 
See also alkaloids; glycoside; saponin. 

honey Honey of any type can contain Clostridium 
botulinum spores, which are harmless to everyone 
except infants under one year of age. For this reason, 
infants should never be fed raw honey of any 
type, since botulism spores can be fatal to this 
group. 

See also botulism; botulism, infant; Clostrid- 
ium BOTULINUM. 



hormone disruptors Researchers are gathering a 
growing amount of evidence that some persistent 
organic pollutants (POPs), such as DDT, dieldrin, 
furans, dioxins, and PCBs, among others, mimic, 
inhibit, and/or disrupt hormones and interfere 
with their natural regulatory processes, even at 
very low doses. These substances are called hor- 
mone disruptors (also endocrine disruptors, xen- 
oestrogens [estrogen disruptors]), and they have 
well-documented negative effects on wildlife and 
reportedly similar effects on humans. 

In animals, for example, hormone disruptors are 
causing feminization of male fetuses, dysfunctions 
in reproductive processes, behavioral changes, and 
development problems. Scientists are seeing exam- 
ples of partially developed male and female sexual 
organs in alligators and polar bears and abnormally 
small genitals in males. In the Great Lakes, herring 
gull nests have twice the number of eggs but they 
are unfertilized and cared for by pairs of female 
birds, because the males have lost interest in the 
natural processes of mating and rearing young. 
Amphibian, reptile, and marine mammal popula- 
tions around the world are declining, possibly due 
to a reduced fertility in males. 

In humans, studies show that hormone dis- 
ruptors may cause ovarian, breast, testicular, and 
prostate cancers; suppress the immune system; 
stimulate early puberty; impair fetal development, 
with the result being smaller babies; reduced intel- 
ligence; hyperactivity and violence; and reduced 
sperm counts. One hormone disruptor, bisphenol- 
A, has been shown to disrupt hormones at very 
low doses in animals and is suspected of causing 
birth defects and reproductive damage that may 
lead to prostate and breast cancer. Bisphenol-A has 
been shown to cause changes in estrogen in animal 
cells at the same concentrations that are found in 
pregnant women and their fetuses. 

Xenoestrogens — substances foreign to the 
human body that directly or indirectly act like 
estrogens — are the most studied of the hormone 
disruptors, primarily because of their apparent 
impact on women's reproductive health. Although 
the majority of the studies have been done in 
animals, the results thus far strongly implicate 
xenoestrogens in disorders ranging from infertility 
to endometriosis, breast and ovarian cancer, birth 



huffing 123 



defects, and premature puberty. Among the more 
commonly recognized xenoestrogens are bisphe- 
nol-A, DDT (banned), endosulphan (not banned), 
and atrazine, the most commonly used weed killer 
for corn in the United States. 

Hormone disruptors are found in a wide range 
of products and in the environment: from solvents 
to detergents, plastics (bottles, bags, wrap, food 
containers), pesticides, industrial chemicals, dry- 
cleaning solvents, carpet, furniture, and byproducts 
of industry. They are also found in foods, including 
milk, soy beans, fish, meat, and poultry, and in 
drinking water. 

See also bisphenol-A, persistent organic 

POLLUTANTS. 



horse chestnut (Aesculus hippocastanum) The 

horse chestnut tree is a native of the Balkan Pen- 
insula but it also grows throughout the Northern 
Hemisphere. Also called Spanish chestnut and 
buckeye (but not to be confused with the Califor- 
nia or Ohio buckeye trees), the seed extract of the 
horse chestnut plant is used throughout Europe 
for chronic venous insufficiency, a condition char- 
acterized by swollen legs, varicose veins, skin 
ulcers, itching, and leg pain. It is also used to treat 
hemorrhoids. 

Poisonous part 

Unprocessed horse chestnut seeds are poisonous, 
as are the leaves, bark, and flowers, all of which 
contain the toxin esculin. Properly processed horse 
chestnut seeds contain little or no esculin. When 
purchasing horse chestnut seed extract, products 
should be standardized to a substance called escin. 

Symptoms 

If poisoning occurs, symptoms include muscle 
twitching, vomiting, diarrhea, headache, confu- 
sion, weakness, poor coordination, coma, paralysis, 
and death. Based on animal studies, horse chestnut 
seed extract may lower blood sugar, and so patients 
with diabetes or hypoglycemia should be cautious 
when using this supplement. Serum glucose levels 
may need to be monitored by a healthcare pro- 
vider. Use of topical horse chestnut may cause skin 
irritation. People with bleeding disorders are cau- 



tioned when using horse chestnut as the herb may 
increase the risk of bleeding. 

Treatment 

Symptomatic. 

horse nettle See Carolina horse nettle. 



huffing Inhalant abuse, also called huffing, sniff- 
ing, and bagging, is the intentional inhalation of 
chemical vapors for the purpose of achieving an 
altered mental and/or physical state. Most of the 
people who practice huffing are adolescents, and 
they are after a euphoric effect to enhance their 
experiences during clubbing and raves. Nearly 3 
million teenagers are believed to practice huffing. 
Adult abusers typically huff to enhance their sex- 
ual experiences. Huffing is widespread across the 
United States, but it may be underreported because 
many people, including healthcare providers, law 
enforcement officials, and parents, are not familiar 
with the signs of inhalant abuse. 

The chemical vapors sought after as inhalants 
for huffing can be found in more than 1,000 com- 
mon products often available in most homes. These 
products fall into some general categories. Aerosols 
are sprays that contain solvents and propellants. 
The most popular among inhalant abusers are sil- 
ver and gold spray paint, deodorant, hair products, 
cooking products, and fabric protector. Gases such 
as medical anesthetics and refrigerants are popu- 
lar. Users turn to butane lighters, air-conditioning 
units, and propane tanks. Laughing gas (nitrous 
oxide) is abused more frequently than any other 
gas, and it can be found in whipped cream dispens- 
ers or products that enhance the octane levels in 
cars. Drug paraphernalia stores also sell sealed vials 
called whippets that contain the gas. 

Volatile solvents are liquids that vaporize at room 
temperature. They include felt-tip markers, nail 
polish and remover, glue (rubber cement), paint 
thinner, gasoline, and correction fluid. Nitrites are 
used primarily to enhance sexual experiences and 
are a group of chemicals that include cyclohyxyl 
nitrite, amyl nitrite, and butyl nitrite. Cyclohexyl 
nitrite is found in room deodorizers; amyl nitrite 



124 hyacinth 



and butyl nitrite are sold in small bottles referred 
to as poppers. 

Symptoms 

Initially users experience excitation, then drowsiness, 
lightheadedness, loss of inhibitions, and agitation. 
Additional effects during or shortly after use include 
dizziness, strong hallucinations, delusions, belliger- 
ence, apathy, and impaired judgment. Long-term 
users may exhibit weight loss, disorientation, lack of 
coordination, irritability, and depression. Withdrawal 
symptoms include sweating, rapid pulse, hand trem- 
ors, insomnia, nausea, vomiting, hallucinations, and 
in severe cases, grand mal seizures. Inhaled nitrite 
users experience dilated blood vessels, increased 
heart rate, excitement, and a sensation of heat. 

Chronic huffing may result in irreversible dam- 
age to the heart, kidneys, lungs, brain, and liver. 
Brain damage may appear as memory impairment, 
slurred speech, and personality changes. Death can 
occur after a single use or prolonged use. Causes 
of death may include heart failure, asphyxiation, 
aspiration, or suffocation. 

Treatment 

If someone is in a state of crisis, stay calm, because 
agitation may cause the user to become violent or 
suffer heart dysfunction, which can result in sudden 
death. Make sure the user is in a well-ventilated 
area and call emergency medical services. Enroll- 
ment in a treatment facility is often recommended. 

hyacinth (Hyacinthus orientalis) A plant widely 
cultivated throughout the United States for its fra- 
grant bell-shaped flowers. 

Poisonous part 

The bulb of this plant is poisonous. 

Symptoms 

Ingestion of the bulb of the hyacinth causes severe 
stomach problems, which, while not fatal, can be 
very painful. 

Treatment 

Perform gastric lavage or induce vomiting; treat 
symptoms. 



hydrangea (Hydrangea) The hydrangea is consid- 
ered to be one of the most poisonous plants. About 
80 species of this common flowering shrub are 
found throughout the entire Western Hemisphere; 
H. macrophylla is the most popular. 

This deciduous mounded shrub can grow to 
be 15 feet, with large oval leaves with toothed 
edges up to 6 inches long, and white, pink, or blue 
flowers in a showy cluster. Flower color usually 
depends on the acidity of the soil, and the color 
grows brown as the flowers age. 

Poisonous part 

All parts of the plant (but especially the flower 
buds) are toxic and contain the poison hydrangin, 
which is believed to produce toxic cyanide com- 
pounds activated by stomach acids. 

Symptoms 

Several hours after ingestion, the glycosides decom- 
pose in the gastrointestinal tract and release the poi- 
son, which causes gastroenteritis and other cyanide 
poisoning symptoms. Cyanosis may develop, and in 
cases of large doses, convulsions, coma and death. 

Treatment 

Gastric lavage followed by a 25 percent solution of 
sodium thiosulfate. In unconscious victims, acido- 
sis should be corrected and shock treated together 
with the administration of oxygen to aid breathing. 
Cyanide antidote should be administered. 

hydrocarbon An organic compound that contains 
primarily hydrogen and carbon atoms, usually of 
biological origin. Hydrocarbons include ethylene, 
acetic acid (vinegar), methylene chloride, formal- 
dehyde, benzene, DDT, PCB, propylene, butylene, 
toluene, and xylene. 

hydrochloric acid (hydrogen chloride) Hydro- 
chloric acid is usually marketed as a solution 
containing 28 to 35 percent by weight hydrogen 
chloride, commonly known as concentrated hydro- 
chloric acid. It is also found in the stomach lining, 
forming part of the stomach juices and is important 
in the digestion of proteins. 



hypochlorite 125 



A fatal dose of hydrocfiloric acid is almost 
impossible to swallow, since the highly corrosive 
nature of the acid would close up the throat. Skin 
absorption or breathing in the vapors can cause 
fatalities, however. The acid produces burns, ulcers, 
and scarring, destroying any tissue it touches. 

Symptoms 

Eye contact will cause blindness; skin contact will 
result in redness, peeling, burns, and scarring. Inha- 
lation will inflame the throat, tongue, and lungs 
and cause coughing, choking, headaches, dizziness, 
and weakness followed some hours later by chest 
constriction, foaming at the mouth, and cyanosis. 
Blood pressure falls while pulse races, as pulmo- 
nary edema is followed by death. 

When ingested, hydrochloric acid can cause 
burning pain, vomiting, bloody diarrhea, low blood 
pressure, swelling of the throat (causing suffoca- 
tion), and a usually fatal peritonitis. 

Treatment 

Administer a mild alkali (such as milk) to neutral- 
ize acid; treat symptoms as they appear. 

hydrogen peroxide This popular antiseptic found 
in most home medicine cabinets is used as a 
mouthwash, to treat infections, and to bleach hair 
and is usually sold in concentrations of 3 percent. 
Toddlers frequently ingest hydrogen peroxide, but 
it is considered to be of low toxicity. It generally 
breaks down in the gastrointestinal tract before 
it can be absorbed in the body; as it decomposes, 
however, it may release large amounts of oxygen, 
causing stomach distention and nausea. 

hydrogen sulfide This is an irritant gas that 
occurs in the presence of decomposing vegetables 
or animals, such as in liquid manure pits, sewers, 
tanneries, fishing boats, or coal mines; its presence 
is announced by the distinctive smell of rotten eggs. 
Hydrogen sulfide is also an industrial byproduct of 
petroleum refineries and blast furnaces. 

Symptoms 

Poisoning with this gas resembles that of cyanide 
and interferes with the body's oxygen supply. In 



mild exposure, it causes painful and reddened eyes, 
blurred vision, and seeing colored halos around 
lights. In higher amounts, it can cause cyanosis, 
confusion, and pulmonary edema; at very high 
levels, it can cause an almost immediate fatal coma. 
In the case of serious poisoning, the fatality rate is 
6 percent. 

Treatment 

Remove the victim from exposure; give oxygen 
and intravenous nitrite therapy. There is no anti- 
dote to hydrogen sulfide poisoning. If the victim 
lives for four days, recovery is likely, although 
there are lingering side effects for months (includ- 
ing lethargy, headache, fatigue, memory loss, and 
lack of initiative). 

hydromorphone The chemical name for Dilau- 
did, this is a potent analgesic used for moderate 
to severe pain available in a wide variety of forms 
(tablet, injection, rectal suppositories, and oral solu- 
tion). It has become a highly abused drug because 
of its euphoric effects. Clinical effects of this drug 
are quite similar to those of morphine at similar 
doses. 

Symptoms 

Chronic use may result in both physical and psy- 
chological addiction, but an overdose — even in 
those who have been chronic abusers — may cause 
breathing problems and death. Acute overdose 
causes depression of the central nervous system, 
convulsions, shock, cardiopulmonary arrest, low 
body temperature, pneumonia, low blood pressure, 
and slow heart rate. 

Treatment 

Induced vomiting is not recommended; however, 
gastric lavage may be performed even several 
hours after ingestion, followed by the administra- 
tion of activated charcoal and a saline cathartic. 
Seizures may be controlled with intravenous diaz- 
epam. Naloxone may be administered. 
See also morphine; narcotics. 

hypochlorite See alkaline corrosives. 



n 



ibuprofen (Trade names: Motrin, Nuprin, Motrin IB, 
etc.) See nonsteroidal anti-inflammatory drugs. 

indane derivatives These insecticides are chemi- 
cals that dissolve readily in fat and include aldrin, 
dieldrin, endrin, kepone, chlordane, and hepta- 
chlor, although chlordane, heptachlor, aldrin, and 
dieldrin have all been banned. Of these, aldrin is the 
most toxic; recent cancer studies in rodents have 
suggested that heptachlor (contained in chlordane) 
is a carcinogen. Food and Drug Administration 
studies suggest that 70 percent of all meat, fish, 
dairy products, and poultry in the United States 
contain residues of these pesticides. 

Symptoms 

After ingestion or skin contamination, acute poi- 
soning causes excitability, tremors, restlessness, 
and convulsions. In animals, lower doses are asso- 
ciated with liver problems; humans with liver dis- 
ease may be more sensitive to indane exposure. 

Treatment 

Gastric lavage followed by saline cathartics. Avoid 
all fats and oils (including milk), since they increase 
the rate of absorption. Administer phenobarbital 
sodium for tremors and barbiturates for convul- 
sions, and provide oxygen if necessary. If the skin 
has been contaminated, wash with soap and water 
immediately to head off skin problems and sys- 
temic absorption. Remove contaminated clothing. 
See also aldrin; chlordane; dieldrin; endrin; 

INSECTICIDES. 

Indian tobacco (Lobelia inflata) [Other names: 
asthma weed, bladderpod, eyebright, lobelia.] This 
deadly poisonous plant with its attractive red. 



white, and blue flowers is found in waste areas, 
along roadsides and in woodland throughout east- 
ern North America, westward to Nebraska and 
Arkansas. Used homeopathically to treat laryngitis 
and asthma, it was also dried and smoked by Native 
Americans. It gets its name from the Flemish bota- 
nist Matthais de UObel. 

Indian tobacco is an annual or biennial rela- 
tive of the bellflowers, with its flowers appearing 
in July and August as loose spikes and alternate, 
toothed leaves. Similar in many aspects to nicotine, 
Indian tobacco has been advertised as a substitute 
for tobacco and as a weight-reducing aid. 

Poisonous part 

The entire plant is poisonous and contains alkaloids 
of lobeline and lobelamine. These toxins act by 
exciting, and then depressing, the central nervous 
system. In limited amounts Indian tobacco can open 
the bronchioles, but in larger amounts it can slow 
breathing and cause a drop in blood pressure. In 
addition, leaves, stems, and fruit cause a skin rash. 

Symptoms 

Quite similar to nicotine poisoning, ingesting Indian 
tobacco causes symptoms within one hour, includ- 
ing nausea, vomiting, weakness, tremors, convul- 
sions, coma, and death. As little as 50 mg of the 
dried plant, or I ml of tincture of Indian tobacco, 
can cause these reactions. 

Treatment 

Gastric lavage, artificial respiration, and the admin- 
istration of atropine and Valium. 
See also nicotine. 

indomethacin (Indocin) See nonsteroidal anti- 
inflammatory DRUGS. 



126 



insecticides 127 



inky cap (Coprinus) The inky cap is the common 
name for the 100 different types of mushroom spe- 
cies of the genus Coprinus, which get their name 
from the fact that after the mushrooms discharge 
their spores, the cap disintegrates into an inklike 
liquid that has been used for writing. The mush- 
rooms are found growing on dung or buried wood, 
and the caps of C. atramentarius and C. comatus 
(shaggy mane or shaggy cap) are edible if picked 
young, before the gills turn black. 

Symptoms 

While these mushrooms are edible, the coprine in 
the mushrooms is similar to disulfiram (Antabuse) 
and interferes with the metabolism of ethanol, 
causing intoxication when alcohol is drunk within 
72 hours of eating the mushroom. The alcohol 
is believed to increase the solubility and absorp- 
tion of the poison and causes giddiness, nausea, 
vomiting, sweating, breathing problems, and even 
tachycardia. Many victims recover within a few 
hours, but eating a large amount of mushrooms 
with alcohol can result in low blood pressure and 
cardiovascular collapse. The reaction persists for 
several hours. 

Treatment 

Supportive, including the administration of intra- 
venous fluids. There is no antidote, and once they 
appear, the symptoms usually fade within several 
hours. 

See also Antabuse; coprine; mushroom poison- 
ing; MUSHROOM TOXINS. 



inocybe mushroom These members of the cort 
family range in toxicity from mild to fairly poison- 
ous, but none is as toxic as the Amanita genus of 
mushrooms. The most dangerous are the Inocybe 
napipes and I. fastigiata. They are found in pine 
forests throughout the United States, with gray- 
brown spores and small, brown caps. 

Poisonous part 

These mushrooms contain the parasympathetic 
stimulant muscarine, which is not affected by 
cooking and affects the autonomic nervous system 
and the liver. 



Symptoms 

Ingesting small concentrations of muscarine is 
associated with sweating and sometimes abdominal 
pain; other symptoms develop rapidly and include 
salivation, cyanosis, weak muscles, twitching, weak 
pulse, delirium, hallucinations, and convulsions, 
but rarely death. Heart attacks occur in only 4 per- 
cent of cases, since treatment is generally started in 
time to prevent this. Intoxication usually subsides 
within two hours. 

Treatment 

Induce vomiting or perform gastric lavage, since 
it is possible to get rid of the poison this way and 
recover quickly. Atropine is the antidote for mus- 
carine poisoning and may be given to those who 
experience severe discomfort or anxiety. 

See also Amanita mushrooms; cortinarius 
mushrooms; muscarine; mushroom poisoning; 
mushroom toxins. 



inorganic chemical insecticides One of four 
major groups of insecticides, the inorganic chemi- 
cal insecticides include arsenic compounds, fluo- 
rides, thallium, selenium, metaldehyde, mercury, 
phosphorus, sodium borate, hydrocyanic acid (cya- 
nide), pyrethroid, and antimony. 

See also antimony; arsenic; cyanide; insecti- 
cides; mercury; metaldehyde; phosphorus; sele- 
nium; THALLIUM. 

insecticides There are many wide-spectrum or 
all-purpose products to kill insects, and in the past 
most were synthetic chemical compounds created 
in laboratories to mimic nature. These products 
were convenient and effective; however, gardeners 
came to recognize that such panaceas carry certain 
penalties — they poisoned more than the insects 
they were designed to attack. 

Today, insecticides fall into two groups: those 
that coat the outside of a plant, and those that are 
absorbed by the roots, stems, or leaves into the 
plant itself. There are six major types: minerals, 
such as kerosene or borax; botanicals or natural 
organic compounds (nicotine, pyrethrin, and oro- 
tenone); chlorinated hydrocarbons (DDT, lindane, 



128 insect repellents 



chlordane); organophosphates (malathion and 
diazinon); carbamates (carbaryl and propoxur); 
fumigants (such as naphthalene) and benzene 
(mothballs, etc.). 

Newer insecticides include insect-growth regu- 
lators and natural predators (such as beetle-eating 
wasps, or insect-killing bacteria). 

While all insecticides are toxic, most fatal poi- 
sonings occur only when large quantities are acci- 
dentally or intentionally ingested or inhaled. 

See also benzene; botanic insecticides; carba- 
mate; chlordane; chlorinated hydrocarbon pes- 
ticides; DDT; lindane; malathion; naphthalene; 
organophosphate insecticides; phosphate esters; 
phosphorus. 



insect repellents Substances that, when applied 
or sprayed on the skin, repel mosquitoes, gnats, 
and other insects. Because these products are 
designed for human use, they are generally con- 
sidered nontoxic, although they are not recom- 
mended for use on small children. While poisoning 
from insect repellents is rare, there have been a few 
cases of toxicity with DEBT (diethyltoluamide). 

insulin Insulin is a hormone produced by the 
pancreas. Supplements of insulin have been used 
to treat diabetes mellitus since 1922; today, they 
are used in all cases of insulin-dependent diabetes 
mellitus, and sometimes for noninsulin-dependent 
diabetes when oral hypoglycemic drugs don't 
work. These supplements are produced from pig 
or ox pancreas and by genetic engineering; there 
are a variety of short-, medium-, and long-acting 
insulins available. Insuhn may either be injected 
by the patient before meals or introduced with an 
insuhn pump to deliver the hormone over a 24- 
hour period. Oral doses of insulin are not absorbed 
and are not toxic. 

Symptoms 

An overdose can cause hypoglycemia (low sugar 
level) with dizziness, sweating, irritability, and 
weakness; severe hypoglycemia coma and perma- 
nent brain damage have occurred following injec- 
tions of 800 to 3,200 units of insulin. 



Treatment 

Administer concentrated glucose as soon as pos- 
sible after drawing blood samples; treat symptoms. 

iodine This element is one of the oldest antisep- 
tics used in medicine, found most often in com- 
pound form as an antiseptic and cough remedy. 
Discovered in 1811, tincture of iodine was first 
used in 1839 by a French surgeon and put to work 
again on the battlefields of the American Civil War. 
It remains a popular choice for home medicine 
cabinets today as an inexpensive skin antiseptic. It 
is also used in contrast dyes for X-rays and fluoros- 
copy, and in making dyes, photo film, water treat- 
ment and medicinal soap. 

The brownish element is not soluble in water 
but dissolves readily in alcohol; it is available in 
solid and tincture preparations. While earning a 
deadly reputation as a serious poison, iodine does 
not often cause toxic poisonings in the amounts 
normally found in the household. Iodoform, iodo- 
chlorhydroxyquin and sodium and potassium 
iodides are all powders or crystals with similar 
solubility. 

Symptoms 

Oral ingestion of iodine produces toxic symp- 
toms similar to those of acid corrosives; absorbed 
through the skin, it is toxic because of its ability to 
be well absorbed through the skin of burn patients 
or neonates. Iodine is a central nervous system 
depressant and also interferes with cellular activ- 
ity. Following ingestion, symptoms include vomit- 
ing, diarrhea, abdominal pain, thirst, shock, fever, 
delirium, stupor, and death. A fatal dose of iodine 
and iodoform is about 2 grams. However, food in 
the stomach inactivates iodine by converting it to 
harmless iodide. Fatalities from iodochlorhydroxy- 
quin and iodide salts are rare. Accidental ingestion 
of the tincture is rarely fatal, since it is not rapidly 
absorbed. 

When iodine is applied to the skin, it can cause 
hypersensitivity in some people, including a fever 
and generalized skin reaction. Because of this 
sensitivity in some individuals, iodophors have 
generally replaced the use of iodine tinctures; one 
of the most widely used iodophors is a complex 



ipecac syrup 129 



of povidone and iodine (Betadine). These iodo- 
phors are compounds of iodine linked to a carrier 
agent. 

Treatment 

After acute ingestion, give milk immediately fol- 
lowed by a starch solution (such as 15 milligrams 
of cornstarch or flour to 500 milhliters of water). 
Vomiting is not advisable if there is any esophageal 
injury, and milk should be repeatedly given every 
15 minutes to ease stomach irritation. Antidote is 
sodium thiosulfate, which reduces iodine to iodide. 
In the event of an allergic reaction, administer epi- 
nephrine and intravenous hydrocortisone. 

ipecac syrup A substance that makes people 
vomit (an emetic), ipecac syrup (also called ipeca- 
cuanha) comes from the dried roots of a poisonous 
shrub (Cephaelis ipecacuanha) found in Europe and 
Central and South America. The commercially 
available syrup is used in the treatment of acciden- 
tal poisoning to remove the toxic substance from 
the stomach before it is absorbed into the blood. 

It is a thick, amber liquid that will stay fresh for 
several years in a tightly closed container stored at 
room temperature. It is available over the counter 
in syrup form but should be kept out of the hands 
of youngsters, as ipecac is poisonous. 

Ipecac syrup should never be given to a sus- 
pected poisoning victim unless instructed to do so 
by a health care speciahst. Not all poisons require 
the removal of the poison, and sometimes vomiting 
can be dangerous — especially if the toxic substance 
is caustic or petroleum based. Syrup of ipecac 
should not be given to anyone not fully conscious 
or to a child under age one without careful super- 
vision. While ipecac syrup saves lives, it is itself 
poisonous and should never be given in more than 
two doses. More may be toxic. 

In a recent study (the first ever done in an emer- 
gency room on pediatric poisonings), researchers 
at Children's Hospital of Buffalo tested whether 
giving ipecac in addition to charcoal would help 
remove poison from the body even better. In that 
study, 32 of 70 children less than six years old at 
the hospital took syrup of ipecac before taking 
activated charcoal; the rest of the group received 



charcoal alone. The children treated with both 
took an average of 39 minutes longer to recover 
than the group treated with charcoal alone. Doc- 
tors had to wait from 30 minutes to two hours 
until the ipecac's work was done and the children 
stopped vomiting so they could administer the 
charcoal. Even then, the queasy feeling caused by 
the ipecac made it more difficult for the children 
to keep from vomiting the gritty charcoal solution, 
while most of the children who took the charcoal 
alone had no problems. 

Because time is so important in the treatment 
of poisoning cases, many scientists now believe 
that activated charcoal alone may be the better 
emergency room treatment. Ipecac only empties 
the stomach of its toxic contents, but by the time 
a child sees a physician in the emergency room, 
it has usually been at least an hour since the poi- 
son was ingested and chances are the poison has 
already traveled into the small intestine. 

Ipecac taken within five minutes of ingestion 
will remove about 50 or 60 percent of the poison, 
which can reduce a substance like aspirin to a safe 
level. But after an hour, only 20 percent of the 
poison will come back up. At that point, activated 
charcoal does a better job, since it can pass through 
the intestine, bind with the poison, and move it out 
of the body through the stool. 

Charcoal, then, may well replace ipecac in hos- 
pitals. At home, however, charcoal is more difficult 
to administer because children don't like the taste- 
less, gritty solution. According to Allan Kornberg, 
M.D., head of the emergency medicine department 
at the Children's Hospital of Buffalo and author of 
the above study, ipecac should continue to be used 
at home for emergencies — but always with the 
guidance of a poison control center. 

While the correct dosage should be prescribed 
by a physician or poison control center, a normal 
dose for a person over age one is two tablespoons 
followed by at least two to three glasses of water, 
not milk. If the victim hasn't vomited within 20 
minutes, the dose may be repeated. If the victim 
doesn't vomit after the second dose, call the poison 
control center for further instructions. If possible, 
the victim should vomit into a container so the 
material can be identified by medical experts at 
the hospital. Vomiting is effective only if it occurs 



130 ipecacuanha 



within four hours of ingestion of a solid substance, 
or within two hours after ingestion of a liquid. 
See also charcoal, activated; ipecacuanha. 

ipecacuanha (Cephaelis ipecacuanha) Ipecacua- 
nha is a poisonous plant found throughout Europe 
and South and Central America and is the plant 
source for ipecac syrup, which is used, ironically, 
as an emetic to rid the stomach of poisons. (When 
used incorrectly, however, this syrup can be fatal.) 
The fluid extract from the plant is 14 times more toxic 
than the commercially available ipecac syrup and should 
never be used as a substitute. 

Poisonous part 

The berries and juice are most toxic and contain 
the alkaloid emetine, which weakens the heart. 

Symptoms 

Vomiting occurs immediately after ingestion but 
may not be fatal until 24 hours to a week later. 
Recovery can take up to a year. 

Treatment 

Gastric lavage, morphine, and bed rest. 
See also ipecac syrup. 

iron in drugs and supplements Dietary supple- 
ments that contain iron (ferrous sulfate, ferrous 
gluconate, ferrous fumarate) are common — but 
overlooked — potential poisons in children. An 
acute overdose of iron can damage the stomach 
and small intestine, affect blood circulation and 
damage the liver and other organs, causing shock 
and even death. Young children have been seri- 
ously injured by swallowing doses of 200^00 mg 
of iron, equivalent to 14 to 27 children's vitamin- 
and-mineral supplements with iron or four to 
seven tablets of a typical adult iron supplement. 
More than 2,000 people are poisoned each year 
with iron, and a large number of these poisonings 
are fatal; mortality may be as great as 50 percent. 
The Food and Drug Administration ruled in 1997 
that packages of all preparations that contain iron 
(such as iron supplements and vitamins) must 
now display a warning that accidental overdose of 



iron-containing products is a leading cause of fatal 
poisoning in children under the age of six. In addi- 
tion, products containing 30 mg or more iron per 
unit must be packaged as individual doses that will 
limit the number of pills or capsules a small child 
could swallow. 

Despite child-resistant packaging, accidental 
overdose of iron remains a common cause of 
poisoning in children under six. According to the 
U.S. Consumer Product Safety Commission, pedi- 
atric iron-related injuries increased 150 percent in 
1986, from an annual average of 1,200 from 1980 
through 1985 to 3,000 from 1986 through 1996. 
The number of accidental overdoses and deaths 
declined dramatically, however, after the U.S. Food 
and Drug Administration (FDA) proclaimed a regu- 
lation for unit-dose packaging of iron supplements 
in 1997. In a study that compared the 10 years 
prior to the regulation with the five years after 
its implementation, the average number of iron 
ingestion calls to Poison Control Centers regarding 
children younger than six years decreased from 
2.99 per 1,000 to 1.91 per 1,000, and the number 
of deaths decreased from 29 to one. 

Iron is used by the body to produce the red 
blood cells that transport oxygen, and it helps the 
cells in the muscles and other parts of the body 
turn oxygen into energy. But recent research by a 
team of Finnish researchers links excess iron stored 
in the body to heart disease. Men who ate iron-rich 
food (such as red meat) faced a higher likelihood 
of heart attack. The findings could help force public 
health experts to rethink dietary recommenda- 
tions for iron ingestion, since even normal levels of 
stored iron may prove damaging. Over-the-coun- 
ter vitamin supplements often contain iron, as do 
some enriched foods such as cereals. 

Up until the late 1800s, iron therapy was used to 
treat anemia, but it later fell out of favor. Recently, 
however, ferrous sulfate has been widely prescribed 
to treat iron deficiency anemia, and its popularity 
has greatly increased the risk of poisoning. There 
are about 120 iron products currently marketed in 
the United States. 

The exact mechanism behind iron poisoning 
is not known, nor is it understood how death 
results — whether from shock, from systemic effects 
due to the passage of large amounts of iron into 



ivy 131 



the blood or from the metabolic effects of absorbed 
iron, which cause respiratory collapse. 

Symptoms 

Within 30 minutes of overdose, the first symptoms 
appear: lethargy, vomiting, fast and weak pulse, 
low blood pressure, shock, pallor, cyanosis, acido- 
sis, clotting problems, and coma. Then, symptoms 
may disappear, and the victim may seemingly begin 
to improve. One or two days later, the victim goes 
into shock, with pulmonary edema, vasomotor col- 
lapse, coma, and death within 12 to 48 hours. 

Treatment 

Control shock; perform gastric lavage with sodium 
bicarbonate and administer a chelating agent. Peri- 
toneal dialysis or hemodialysis, or early exchange 
transfusion, may be needed. Give supportive and 
symptomatic therapy as required, including mul- 
tiple vitamins and antibiotics. 
See also vitamins. 



irritant oils Some glycosidal oils in high concen- 
trations can irritate the digestive tract. While in 
small quantities they are harmless (such as the oils 
in plants of the mustard family, horseradish, and 
radishes), in large amounts they are more upsetting 
and cause the irritations found with some plants of 
the buttercup family and anemone species. 
See also volatile oils. 



isopropanol See isopropyl alcohol. 

isopropyl alcohol Widely used as a solvent, antisep- 
tic, and disinfectant, isopropyl alcohol (also known 
as isopropanol) is found in products such as shaving 
lotions and window cleaner and is twice as toxic as 
its relative ethyl alcohol. It is also found in the home 
as a 70 percent solution (rubbing alcohol), which is 
commonly drunk by alcoholics as a substitute for 
liquor. But unlike other common alcohol substitutes 
(methanol and ethylene glycol), isopropyl alcohol is 
not metabolized to highly toxic organic acids. 

While the effects of isopropyl poisoning resemble 
drunkenness, they may last up to four times longer 



than those induced by alcoholic drinks. Rubbing 
alcohol can be swallowed, inhaled (as a vapor), or 
absorbed. In fact, alcohol sponge baths were once 
prescribed as a way to reduce fever, until it was 
discovered that the alcohol sometimes produced a 
nonfatal coma. 

Isopropyl alcohol is a potent central nervous 
system depressant, and ingestion or inhalation of it 
can cause coma and respiratory arrest. It is metabo- 
lized to acetone, which may contribute to and pro- 
long the central nervous system depression. 

Symptoms 

Within 10 to 30 minutes after ingestion (depending 
on how much food is in the stomach), overdose 
symptoms appear: nausea, vomiting, stomach pain, 
depressed respiration, vomiting blood, excessive 
sweating, hemorrhage in the trachea and bronchial 
tubes, pneumonia, swelling, and coma. 

Treatment 

There is no specific antidote. Ethanol is not given 
as an antidote, and if the victim has only drunk a 
few swallows or more than 30 minutes has passed, 
there is no point to emptying the stomach, since 
the alcohol is rapidly absorbed after ingestion. 

However, for large ingestions, perform gastric 
lavage (do NOT induce vomiting) and adminis- 
ter activated charcoal and a cathartic, although 
charcoal will not absorb isopropyl alcohol very 
well. Hemodialysis removes isopropyl alcohol and 
acetone, but it is usually not necessary because 
the majority of victims can be managed with sup- 
portive care alone. Dialysis is indicated when levels 
are very high, or if low blood pressure does not 
respond to fluids. 

See also ethanol; ethyl alcohol; methanol. 

isoproterenol This drug, similar to catechol- 
amines, is useful in the treatment of excessively 
slow heartbeat following an overdose of beta 
blockers. 

See also beta adrenergic blockers. 



ivy (Hedera) Of the five species in the genus 
Hedera, H. helix (English ivy) is the most common. 



132 ivy 



This form is poisonous if eaten because of tfie pres- 
ence of saponins; in small amounts it can cause 
stomach upset and a tingling sensation around 
the mouth, but large amounts can lead to labored 
breathing, convulsions, and coma. While no fatal 
cases have been reported in the United States, 
European children have been poisoned with this 
plant. 

English ivy is a climbing evergreen plant with 
three- or five-lobed leaves and a woody stem and 
prefers shade and damp, moist ground. Occasion- 
ally, it produces black berries. There are more than 
200 cultivars, and ivy has been a known toxicant 
since early Greek times. 



Poisonous part 

All parts of the ivy plant contain the saponin 
hederin and are poisonous if eaten. 

Symptoms 

Burning sensation in the throat, nausea, vomit- 
ing, diarrhea, excitement, difficulty in breathing, 
abdominal pain, excess salivation, and skin irrita- 
tion; rarely, it causes coma. 

Treatment 

Traditional treatment of gastroenteritis and fluid 
replacement, especially in young children. 
See also saponin. 



jack-o'-lantern fungus (Clitocybe illudens) This 
cousin of the Inocybe mushroom also contains 
muscarine and induces sweating. An orange fun- 
gus found growing on wood, it can induce severe 
vomiting but is not fatal. 

Symptoms 

This fungus can cause gastrointestinal upset. Inges- 
tions of small amounts of the parasympathetic 
stimulant muscarine contained in these mush- 
rooms also cause vomiting and blurred vision. 

Treatment 

Intoxication usually subsides after two hours; 
when the victim experiences severe discomfort or 
anxiety, atropine may be given. Other treatment is 
symptomatic. 

See also inocybe mushroom; mushroom poison- 
ing; MUSHROOM TOXINS. 

jellyfish Although the term is used to refer to 
any marine member of a group of invertebrates, 
the true jellyfish family includes about 200 species, 
all of which are disk- shaped animals found drifting 
along the shoreline. Jellyfish, together with cor- 
als, sea anemones, and Portuguese men-of-war all 
belong to the group of marine animals called coel- 
enterates, which have four, eight, or more dangling 
tentacles with capsules that sting when touched. 

Most common in tropical waters, jellyfish float 
on the surface of the water, traihng tentacles that 
can penetrate human skin and inject venom. Most 
live for only a few weeks, but some live as long as 
a year, and the deep-sea species may live longer. 
Jellyfish are by far the most common of the coel- 
enterates and cause a significant number of injuries 
in the United States coastal areas. 



Produced in a wide variety of sizes, colors, and 
shapes, jellyfish often are almost transparent with 
brilliant tentacles, ranging from a few millimeters 
to more than two meters across the top. Because 
some varieties have such long tentacles, it is pos- 
sible to be stung without ever seeing the top of the 
jellyfish floating on the surface. Jellyfish are also 
dangerous after storms have broken them up and 
sprinkled them across the sandy beaches, where 
they can still sting — even when dry. 

One of the most poisonous of the jellyfish is 
the sea wasp (Chironex fleckeri) which swims from 
Queensland north to the central Atlantic coast of 
the United States; a moderate sting from a sea wasp 
can cause death within a few minutes. While most 
stings from poisonous fish and jellyfish may not 
cause much harm, some jellyfish and Portuguese 
men-of-war can inflict severe stings, and the victim 
may panic and drown. The lion's mane jellyfish 
(Cyanea capillata) is the giant of all jellyfish, with a 
sac that reportedly measures 8 feet or more across. 
Its tangle of poisonous tentacles arranged in groups 
of eight (each group with 150 tentacles) may reach 
over 100 feet long. The lion's mane ranges in the 
Atlantic and Pacific Oceans, and although it is not 
beheved to be fatal to humans, its sting is very 
painful. The most common jellyfish is the moon 
jellyfish (Amelia aurita), which is only slightly ven- 
omous and is found in all warm and temperate 
waters. 

Symptoms 

Stings from a jellyfish cause severe burning pain 
and a red welt — or a row of lesions — at the site of 
the sting. Some victims also suffer from headache, 
nausea, vomiting, muscle cramps, diarrhea, con- 
vulsions, and breathing problems. In the water, the 
initial shock of the sting may cause a swimmer to 



133 



134 Jerusalem cherry 



jerk away, which stimulates the tentacles to release 
more poison. On shore, more poison is released 
if the victim tries to rip off the sticky threads. On 
those who have been stung by jellyfish but survive, 
the wounds from the jellyfish stings become red 
bfisters that can leave permanent scars. One or two 
weeks after the sting, the victim may experience a 
recurrence of the lesions at the site, which can be 
treated with antihistamines. 

In the United States, it is not particularly impor- 
tant to identify the type of coelenterate, but in 
Austrafia (where many lethal varieties exist) it is 
crucial. 

Treatment 

Alcohol, ammonia, or vinegar and salt water (do 
not use freshwater) poured over the site of the sting 
will deactivate the tentacles, which should then 
be scraped off with a towel or with sand held by a 
bath towel — not the hand. Pull off — do not rub — the 
tentacles. The tentacles will continue to discharge 
their stinging cells (nematocysts) as long as they 
remain on the skin. Watch carefully for signs of 
shock or breathing problems. 

Baking soda in a paste with water should be 
applied to the sting to refieve pain; after an hour, 
moisten again and scrape off the baking soda with 
an object to remove any remaining nematocysts. 
Calamine lotion also will help ease the burning sen- 
sation, and painkillers may help with the stinging 
pain. (Other local remedies for pain include meat 
tenderizer, sugar, ammonia, and lemon juice.) 

Jellyfish often cause allergic reactions, which 
can be eased by the administration of Benadryl or a 
steroid. A severe reaction to the sting requires hos- 
pitalization and perhaps CPR. Antivenin, effective 
against more dangerous species, may be available 
but must be administered immediately together 
with a tourniquet. Another type of jellyfish, the 
Portuguese man-of-war, is rarely fatal but causes 
hives, numbness, and severe chest, abdominal, and 
extremity pain. If given early, the calcium blocker 
verapamil may be effective. 

See also Portuguese man-of-war. 



Jerusalem cherry (Solanum pseudocapsicum) One 

of the nightshade family, this popular houseplant 



has luscious orange or red berries that are deadly 
poison. It is a decorative pot plant and has escaped 
from cultivation in Hawaii and the Gulf coast 
states. 

Poisonous part 

Human poisoning is usually attributed to immature 
fruit, which contains the toxin solanine glycoalka- 
loid, the poison of the true nightshades. 

Symptoms 

While there is little danger of fatal poisoning in 
adults, children may ingest a fatal amount of this 
plant. Symptoms appear several hours after inges- 
tion and include gastric irritation, scratchy throat, 
fever, and diarrhea (solanine poisoning is often 
confused with bacterial gastroenteritis). 

Treatment 

Provide the same general supportive care that would 
be given in gastroenteritis cases; fluid replacement 
may be required. 

See also nightshade, deadly. 

jessamine, yellow (Gelsemium sempervirens) Also 
known as Carolina jessamine, this plant is a highly 
toxic member of the olive family which has about 
300 tropical and subtropical species of fragrant, 
flowering shrubs. The plants are found in wood- 
lands and are native to all continents except North 
America. Still, it is found today from eastern Vir- 
ginia to Tennessee, and Arkansas south to Florida 
and west to Texas; it is also grown in parts of 
California. 

A perennial evergreen with lance-shaped leaves 
and fragrant, bright yellow flower clusters, the 
plant has a small fruit capsule with winged seeds. It 
is not a member of the jasmine species (Jasminum), 
which causes only a mild skin rash. 

Poisonous part 

All parts of this plant contain the poisons gelse- 
mine, gelsemicine and other related alkaloids, 
which cause strychninelike effects. There are cases 
of children who were poisoned after sucking on the 
flowers; honey made from the nectar of this plant 
has been impficated in three deaths. 



jimsonweed 135 



Symptoms 

At high doses, poisoning can be fatal in 10 min- 
utes, but it may take several hours in lower doses. 
Symptoms include frontal headache, dizziness, 
drooping eyelids, sweating, weakness, convulsions, 
anxiety, difficulty in breathing, depression, and 
death through respiratory failure. 

Treatment 

Immediate gastric lavage with instillation of a 
slurry of activated charcoal, intravenous fluids, and 
respiratory support. 
See also gelsemine. 

jimsonweed (Datura stramonium) [Other names: 
apple of Peru, devil's trumpet, Jamestown weed, 
mad apple, stinkweed, thornapple.] Responsible 
for more poisonings than any other plant, jimson- 
weed is an extremely deadly member of the potato 
family. Originally called "Jamestown weed," it got 
its name in 1666 following a mass poisoning in the 
town when starving soldiers ate the berries of the 
plant. Jimsonweed is found throughout much of 
the Northern Hemisphere in roadside and waste 
places but never in mountains or woods. 

An annual, jimsonweed grows to about six 
feet with ovate, unevenly toothed, strong-scented 
leaves; large, white or violet trumpet-shaped flow- 
ers; and a large, spiny fruit (often called a thor- 
napple). Seeds are small and dark brown or black 



when ripe and yield what is called "datura." 
Jimsonweed is the source for the alkaloidal drug 
hyoscyamine. There are about 15 species of Datura, 
and while all are poisonous, their fragrance can be 
sweet or unpleasant depending on the season. 

Poisonous part 

All parts of this plant are poisonous and harbor bel- 
ladonna alkaloids (the poisons hyoscyamine, hyo- 
scine, and atropine). The juices, seeds, and wilted 
leaves are especially deadly. Four to five grams of 
crude leaf or seed will be a fatal dose for a child. 
Poisonings have occurred from sucking nectar from 
the flower tube or eating fruits containing the poi- 
sonous seeds. 

Symptoms 

Within several hours after ingestion, the first symp- 
toms appear: excessive thirst and dry mouth, dilated 
pupils, dry, hot and flushed skin, headache, vertigo, 
weak pulse, visual difficulty, fever, hallucinations, 
disorientation, urinary retention, decreased bowel 
activity, high blood pressure, delirium, convul- 
sions, coma, and death. Handling the leaves and 
rubbing the eyes can dilate the pupils. 

Treatment 

Sedatives are effective for convulsions, and a pur- 
gative may also be used. If intoxication is severe, 
slow intravenous administration of physostigmine 
is usually advised until symptoms diminish. 



K 



kepone See mirex. 

kerosene See petroleum distillates. 



ketamine "Special K," or ketamine hydrochlo- 
ride, is a powerful hallucinogen that was developed 
for veterinary use but which has become a drug of 
abuse. Ketamine causes powerful hallucinations 
that are accompanied by visual distortions and a 
lost sense of time, identity, and sense. The high can 
last from 30 minutes to two hours, but the drug 
can still affect the body up to 24 hours later. It is 
available as a powder that is usually snorted, but 
it can be sprinkled on marijuana or tobacco and 
smoked. Some users combine it with other drugs, 
including heroin, cocaine, or ecstasy. 

Liquid ketamine was developed in the early 
1960s, and it was used as an anesthetic during 
the Vietnam War. The powdered version of the 
drug became popular as a recreational drug in the 
1970s, and it has stayed on the drug scene ever 
since. Because it is odorless and tasteless, it can be 
added to beverages without being detected, and so 
it is sometimes used as a date rape drug. It is simi- 
lar molecularly to phencyclidine (PCP) and thus 
produces similar effects. Because ketamine is an 
anesthetic, users do not feel pain, and this feature 
can lead users to inadvertently injure themselves. 

Symptoms 

Beyond the acute effects of the drug, use can result 
in serious physical and mental problems includ- 
ing delirium, amnesia, impaired motor function, 
depression, high blood pressure, muscle rigidity, 
aggressive/violent behavior, slurred speech, numb- 
ness, and potentially fatal respiratory disturbances. 



Low doses (25-100 mg) produce psychedelic effects 
rapidly; larger doses can produce vomiting and con- 
vulsions. One gram can cause death. Some people 
experience flashbacks up to one year after use. 

Treatment 

Symptomatic; there is no antidote. 

kokoi frog One of the "arrow poison" frogs, this 
frog has a venom in its skin that has been used for 
centuries as an arrow poison by the Cholo Indians 
of Colombia. Ten times more deadly than the toxin 
found in the Japanese pufferfish, it is the most 
active venom known. The molecular structure of 
the toxin found in the kokoi frog is related to that 
of steroid hormones secreted by the adrenal gland. 

Symptoms 

The toxin in the kokoi frog blocks the transmission 
of nerve impulses to the musculoskeletal system, 
causing death within minutes. 

Treatment 

There is no known antidote. 
See also arrow poison frogs. 

krait, blue (Bunguras coeruleus) This is one of 
the nonhooded members of the cobra family; it has 
powerful venom but seldom bites humans. Still, of 
those who are bitten, nearly half die if untreated. 
The krait is generally passive and has shiny scales 
and bands of yellow and black, or white and 
black. 

Similar to the blue krait is the banded krait, 
or pama (B. fasciatus), also a member of the cobra 
family. This variety is almost harmless, although 



136 



krait, blue 137 



larger than its blue krait cousin. While the venom 
is lethal, bites are very rarely reported. 

The kraits are fairly small and are mainly noc- 
turnal; when disturbed, they tend to roll up into a 
loose ball and only bite under great provocation. 
They are found throughout most of southern Asia 
and range from 4 to 7 feet long with light and dark 
bands and short fangs. 

Symptoms 

The venom of snakes in the cobra family contains a 
neurotoxin chemically different from that of other 
snakes. While there is little local reaction, within 1 5 
to 30 minutes more generalized symptoms appear: 



pain, swelling, a drop in blood pressure and confu- 
sion followed by death if the poison spreads to the 
respiratory muscles. The venom from this snake 
family is twice as toxic as strychnine and nearly five 
times more toxic than that of a black widow spider. 

Treatment 

Immediate administration of specific antivenin — 
only the specific antiserum for the type of cobra 
involved should be used. Many types of antivenins 
are available for the krait bite in southern Asia; 
other antivenins are produced in Bangkok for both 
the blue krait and the pama. 

See also antivenin; cobra; snakes, poisonous. 



L 



labetalol This drug is used in the treatment of 
high blood pressure and racing heartbeat associated 
with stimulant drug overdose (such as cocaine or 
amphetamines). 

laudanoisine See morphine. 



laudanum A solution of opium once used as a 
sedative and painkiller and to treat diarrhea. It was 
created in the 16th century by the Swiss physician 
Paracelsus, and it was a popular medication during 
Viaorian times, when physicians would prescribe 
it for women suffering from "the vapors." Elizabeth 
Barrett Browning, Charles Baudelaire, Theophile 
Gautier, Alexandre Dumas, Edgar Allan Poe, and 
Samuel Taylor Coleridge were all users of laudanum; 
in fact, Coleridge wrote his poem "Kubla Khan" 
while in an opium reverie. Unfortunately, the plea- 
surable effects that laudanum brought came at a cost: 
long, dry spells in their creativity and occasional loss 
of ambition. In order to achieve the euphoric effects, 
they had to risk overdose and addiction. 

See also heroin; morphine; narcotics; opium. 

laughing gas See nitrous oxide. 

laurel, mountain (Kalmia latifolia) [Other names: 
Alpine laurel, calfkill, calico bush, hook heller, ivy 
bush, lambkill, mountain ivy, narrow-leaved laurel, 
pale laurel, poison laurel, sheep laurel, spoonwood, 
swamp laurel.] Like its cousin the rhododen- 
dron, the evergreen mountain laurel is a deadly 
narcotic poison found in moist areas and rocky 
hills throughout North America. Ancient Greek 



legends reported that these two plants poisoned 
Xenophon's army when they consumed honey 
made from the flowers' nectar. Closer to home, the 
Delaware Indians used wild laurel for suicide. 

The ornamental bush grows to heights from 
four to eight feet, with three-inch-long leaves and 
white, pink, or purple flowers appearing in June 
and July. The leaves may also be poisonous to ani- 
mals, which in turn can poison any other human 
or animal who eats the meat. Native to North 
America, the plant is not a true laurel but a mem- 
ber of the heath family. 

K. latifolia grows in the northeastern United 
States but not in Canada; K. angustifolia grows in 
eastern North America from Ontario to Labrador 
east to Nova Scotia, and south to Michigan, Vir- 
ginia, and Georgia; K. microphylla is found from 
Alaska to central California. 

Poisonous part 

All parts of the plant are poisonous, especially the 
leaves and nectar (in honey), and contain carbohy- 
drate andromedotoxin, the same poison as rhodo- 
dendron. A tea made from two ounces of the leaves 
of the laurel has caused poisoning. 

Symptoms 

Usually beginning within six hours, they include 
severe gastrointestinal distress, watery eyes and 
mouth, respiratory problems, and bradycardia fol- 
lowed by depression, convulsions, paralysis, coma, 
and death. Death from mountain laurel poisoning 
may occur anywhere from several hours to days after 
ingestion. Children can be poisoned by eating leaves. 

Treatment 

Gastric lavage, fluid replacement, and respiratory 
support; atropine for bradycardia and ephedrine 



138 



lead poisoning 139 



for hypotension that does not respond to fluid 
replacement. 

See also rhododendron. 



laxatives A group of drugs used to treat constipa- 
tion. There are a variety of types of laxatives, each 
causing different symptoms in overdoses. They 
include bulk forming, stimulant, lubricant, and 
saline. In addition, chronic overuse can produce 
bowel function dependency. 

Symptoms 

Stimulant laxatives may cause abdominal cramps 
and flatulence; prolonged use of saline laxatives is 
likely to cause a chemical imbalance in the blood. 
Lubricant laxatives may coat the intestine and 
prevent vitamin absorption. Resulting diarrhea 
from laxative overdose causes fluid and electrolyte 
imbalance. 

Treatment 

Since systemic absorption is not really a problem, 
laxative overdose is simply treated by reestabhsh- 
ing the fluid and electrolyte imbalance caused by 
diarrhea. In cases where the patient is at risk for 
dehydration, perform gastric lavage or induce vom- 
iting followed by the administration of activated 
charcoal. 



lead poisoning Lead poisoning in adults is rare, 
but unfortunately it is one of the most common 
and preventable childhood health problems today. 
It can be a problem for those who lick or eat flakes 
of old paint containing lead. Lead can also contami- 
nate water flowing through old lead pipes, slowly 
poisoning those who drink it. Lead poisoning 
causes the most damage to the brain, nerves, red 
blood cells, and digestive system and is considered 
to be a cumulative poison, since it remains in the 
bones for as long as 32 years and in the kidneys for 
seven. Several recent studies have also shown that 
high levels of lead in the blood can hinder a child's 
growth, and this may occur early in the chemical 
chain of events regulating bone growth — perhaps 
in the brain. 



Symptoms 

Lead is excreted very slowly from the body, so it 
builds up in tissues and bones and may not even 
produce detectable physical effects, although it can 
still cause mental impairment. If they do appear, 
early symptoms include listlessness, irritability, loss 
of appetite and weight, constipation, and a bluish 
hne in the gums followed by clumsiness, vomiting, 
stomach cramps, and a general "wasting." Acute 
poisoning symptoms include a metallic taste in the 
mouth, abdominal pain, vomiting, diarrhea, col- 
lapse, and coma. Large amounts directly affect the 
nervous system and cause headache, convulsions, 
coma, and, sometimes, death. 

Treatment 

Individuals with suspected lead poisoning should 
be given a simple blood test, which can deter- 
mine the level of lead in the blood. A person 
with enough absorbed lead in the body to show 
symptoms will probably require hospitalization. 
Treatment usually includes the administration of 
medicines (called chelating agents) to help the 
body rid itself of lead. In mild cases, the chelating 
agent penicillamine may be used alone; otherwise, 
it may be used in combination with edetate cal- 
cium disodium and dimercaprol. In acute cases, 
perform gastric lavage. 

Prevention 

There are many steps you can take to ensure lead is 
not a problem for you and your family. 

• To temporarily reduce lead paint and dust, clean 
floors, windowsills, and window wells at least 
twice a week with a trisodium phosphate deter- 
gent available at hardware stores. Sponges used 
for this purpose should not be used for anything 
else. 

• Move cribs and playpens away from chipped or 
peeling paint, mantels, windowsills, and doors. 
Replace or strip baby furniture that may be deco- 
rated with lead paint. 

• Wash the child's hands, face, bottle nipples, and 
toys often 

• Children and pregnant women should not be in 
the area while lead paint is being removed. 



140 lepiota mushrooms 



LEAD POISONING GUIDE 

Recommendations by the U.S. Centers for Disease Control and Prevention. 


Lead levels 


Complications 


Treatment 


0-9 mcg/dl* 


None 


Annual checks until age six 


10-14 mcg/dl 


Borderline (possible test inaccuracy); risk for 
mild developmental delays even without 
symptoms 


Nutrition; housecleaning changes will bring 
level down 


15-19 mcg/dl 


Risk for IQ decrease; no symptoms usually 
noticed 


Test for iron deficiency; nutrition; housekeep- 
ing changes will lower level 


20-44 mcg/dl 


Risk of IQ impairment increases; usually no 
symptoms 


Complete medical evaluation; eliminate lead; 
drug treatment possible 


45-69 mcg/dl 


Colic; anemia; learning disabilities 


Remove from home until lead is removed; drug 
treatment 


70 mcg/dl 


Vomiting; anemia; critical illness 


Immediate hospitalization; lead removal 



* mcg/dl - micrograms per deciliter of blood 



• Avoid imported canned foods; the seams of the 
cans may be soldered with lead, which can seep 
into the contents. 

• Feed your child plenty of calcium, iron, and pro- 
tein, with plenty of milk, breads, low-fat foods, 
and green leafy vegetables (they diminish lead's 
effects in the body). 

• Limit the amount of dirt tracked into the house. 
Leave your shoes at the door or make sure 
everyone wipes their shoes on a heavy-duty 
mat in front of the door before they enter the 
house. 

• If you are pregnant, do not drink out of ceramic 
mugs. 

• Test your water's lead levels: it should not exceed 
1 5 parts per billion. 

• Avoid storing acidic food (such as orange juice 
and tomatoes) in ceramic or crystal containers, 
which may contain lead glaze. 

• Never boil water to eliminate lead; boiling only 
concentrates lead. 

• Allow water to run on cold for a few minutes 
before using; never cook with hot water from 
the tap, especially when making baby food, since 
lead leaches more quickly into hot water. 

• If your soil tests high in lead, cover with clean 
soil and seed or sod. 



• Consider a water-treatment device to remove 
lead from tap water. 

lepiota mushrooms (Lepiota josserandii, L. brun- 
neoincarnata, L. helveola, L. subincarnata) The 

poisonous mushroom L. josserandii contains the 
deadly poison amatoxin, and the others in the 
Lepiota genus are assumed to contain amatoxins 
as well. Amatoxins prevent protein synthesis and 
cause cell death, sometimes affecting the kidneys 
as well. These mushrooms are not made less toxic 
by drying, cooking, or boiling in water. 

Symptoms 

Initial symptoms are caused by amatoxin on the 
intestine. After about 12 hours following inges- 
tion, the victim experiences persistent nausea and 
vomiting, intestinal pain, and watery diarrhea. 
This is followed by a period of remission of up 
to five days, followed by liver problems similar 
to those caused by acute viral hepatitis. Without 
treatment, liver and kidney damage cause coma 
and death. 

Treatment 

Give fluids and monitor electrolytes; maintain 
urine flow, since amatoxins are partially excreted 
by the kidneys. Give repeat doses of activated 



lindane 141 



charcoal with water. If the patient was diagnosed 
promptly, massive doses of penicillin may help 
prevent liver damage. In more severe cases, liver 
transplant may be necessary. For most patients, full 
recovery is unlikely. 

See also amatoxins; mushroom poisoning; 

MUSHROOM toxins. 

Librium See benzodiazepines. 

lidocaine A local anesthetic related to cocaine, 
this is a synthetic version of the coca bush alka- 
loids. It is used to control possible irregular heart- 
beat following poisoning by a variety of heart drugs 
and toxins (such as digoxin, cyclic antidepressants, 
stimulants, and theophylline). It is also used to 
relieve pain and irritation caused by sunburn or 
hemorrhoids, to numb tissues before minor sur- 
gery and as a nerve block. It is used topically to 
relieve pain when inserting needles, and it is given 
intravenously as an antiarrhythmic agent following 
a heart attack to reduce the danger of ventricular 
arrhythmias (irregular heartbeat). 

Although lidocaine is used to treat poison- 
ing by other drugs, it is also toxic itself if used 
excessively. 

Symptoms 

Immediately upon ingestion, lidocaine causes gid- 
diness followed by dizziness, blue color, low blood 
pressure, tremors, irregular and weak breath- 
ing, collapse, coma, convulsions, and respiratory 
arrest. 

Treatment 

Efforts to remove the drug after 30 minutes are 
useless. The ingested drug must be removed, and 
absorption from the injection site limited by tour- 
niquet and wet cloths. Give oxygen and artificial 
respiration until the nervous system depression 
lifts. If the victim survives for one hour, recovery 
outlook is good. 

See also antidepressants; digoxin; theophylline. 

lighter fluid See petroleum distillates. 



lily of the valley (Convallaria majalis) Often mis- 
taken for wild garlic, the beautiful white-flowered 
plant is deadly — even the water in which the flowers 
are kept is toxic. Found throughout western North 
America through the Midwest and into Canada 
and Britain, the plant also occasionally bears 
orange-red berries. It is a hardy perennial, with 
hanging, bell-shaped white flowers and smooth, 
dark green leaves, and spreads by underground 
roots to form thick beds. 

Poisonous part 

All parts of this plant are poisonous, especially the 
leaves. The poison, which is similar to digitalis, is a 
glycoside called convallatoxin; the plant also con- 
tains irritant saponins. 

Symptoms 

Immediately after ingestion, the following symp- 
toms appear: nausea, rash, headache, and halluci- 
nations. If large amounts are eaten, dizziness and 
vomiting may occur one or two hours later; slow 
heartbeat can lead to coma and death from heart 
failure. 

Treatment 

Gastric lavage together with cardiac depressants to 
control cardiac rhythm. Activated charcoal may be 
given and repeated later, and saline cathartics may 
also be used. 

See also glycoside; saponin. 

lindane The common name for cyclohexane 
hexachloride, this is a synthetic organic insecti- 
cide used to control insects resistant to DDT and 
those that attack cotton. A cancer-causing agent, 
lindane was formerly used as a general-purpose 
insecticide against indoor pests. The Environmen- 
tal Protection Agency canceled the registration of 
all indoor fumigating devices containing lindane 
in 1986. 

Symptoms 

Less serious poisoning incidents will result in nau- 
sea, dizziness, headache, tremor, and weakness. 
Acute cases of ingestion or skin contamination 
cause vomiting and diarrhea, excitability, loss of 



142 lionfish 



balance, and convulsions. If the insecticide also 
contains an organic solvent, symptoms may also 
include breathing problems and cyanosis followed 
rapidly by circulatory failure. Exposure to the 
fumes from a thermal insecticide vaporizer can 
cause eye, ear, nose, or throat irritation in addition 
to the above symptoms. While symptoms will fade 
after exposure ends, there have been reports of the 
development of anemia. 

Treatment 

Gastric lavage followed by saline cathartics. Avoid 
all fats and oils (including milk), since they increase 
the rate of absorption. Administer phenobarbital 
sodium for tremors and barbiturates for convul- 
sions, and provide oxygen if necessary. If the skin 
has come in contact with these insecticides, wash 
with soap and water immediately to head off skin 
problems and systemic absorption. Remove con- 
taminated clothing. 

See also DDT; insecticides; pesticides; synthetic 

ORGANIC INSECTICIDES. 



lionfish (Pterois) [Other names: butterfly cod, fire- 
fish, rock perch, turkeyfish.] The lionfish includes 
any of several species of the scorpion fish family 
often found off the beaches in Barbados, where 
it hides in coral and stings unwary swimmers. 
Lionfish are famous for their poisonous fin spines, 
which can produce a painful sting that is not usu- 
ally fatal but extremely uncomfortable. The fish 
have 18 spines along their back, which sometimes 
break off in the wound, leading to secondary infec- 
tions and sometimes gangrene. Unaggressive fish, 
they drift peacefully along the coral reefs in which 
they live. 

Symptoms 

Perspiration, rapid heartbeat, vomiting, diarrhea, 
and intense abdominal pain. The wound site is 
swollen, inflamed, and painful, with the pain radi- 
ating outward. 

Treatment 

Supportive; local anesthetic can ease pain around 
the wound site. 

See also scorpion fish. 



listeriosis A rare but potentially fatal illness 
caused by eating food contaminated by the toxic 
Listeria monocytogenes bacterium. It is one of the 
most dangerous foodborne illnesses a pregnant 
woman can contract, causing conditions that 
lead to miscarriage or illness in newborns. The 
government estimates that there are about 2,500 
cases of listeriosis each year, and 500 deaths. 
Some studies have suggested that as many as 
10 percent of all Americans carry the bacteria in 
their intestines. 

While pregnant women are most at risk, others 
at high risk include people with a compromised 
immune system, cancer patients (especially leu- 
kemia patients), the elderly, or people with dia- 
betes, cirrhosis of the liver, asthma, or ulcerative 
colitis. 

There have been outbreaks in Mexican-style 
cheese in California that led to numerous stillbirths 
and a cluster of cases in Philadelphia. The bacteria 
may be found in unpasteurized milk, imported soft 
cheese, hot dogs, lunch meats and spreads, raw 
vegetables, fermented raw-meat sausage, raw and 
cooked poultry, raw meats, and raw or smoked 
fish. One recent study found that 20 percent of hot 
dogs tested contained the bacterium. When listeria 
is found in processed products, the contamination 
probably occurred after processing (rather than 
due to poor heating or pasteurizing). 

Symptoms 

Illness occurs within three weeks after consuming 
tainted products; most healthy people probably 
won't show any symptoms. If they do appear, 
symptoms resemble those of the flu, including a 
persistent fever. Nausea, vomiting, and diarrhea 
may precede more serious forms of listeriosis or 
may be the only symptoms. In high-risk individu- 
als, the infection may spread to the nervous sys- 
tem, causing a type of meningitis including intense 
headache, fever, stiff neck, confusion, loss of bal- 
ance, or convulsions. Listeria meningitis carries a 
fatality rate that may reach 70 percent. 

Diagnosis 

Listeriosis can be diagnosed from a blood test, cere- 
brospinal fluid, or stool. There is no routine screen- 
ing test for susceptibility during pregnancy. 



loquat 143 



Treatment 

Antibiotics are most helpful in pregnant women to 
prevent disease in the fetus. Babies with listeriosis 
receive the same antibiotics as adults, although a 
combination of antibiotics may be used until diag- 
nosis is certain. Even with prompt treatment, some 
infections result in death, especially in those with 
other serious medical problems. 

Complications 
Internal abscesses, meningitis, blood poisoning. In 
pregnant women, the infection can lead to stillbirth 
or miscarriage. 

Prevention 

Pregnant or high-risk patients should avoid foods 
linked to contamination in the past and should 
practice good food preparation practices and wash 
all vegetables and salads well. 

lithium Available either as a pill (lithium carbon- 
ate) or liquid (lithium citrate), this is the treatment 
of choice for manic-depression (bipolar disorder), 
for which it is given orally. It is also used to treat 
alcohol poisoning and schizoid personality disor- 
ders, and sometimes to boost the white blood cell 
count in persons with leukopenia. 

However, toxic levels can be quickly reached, 
causing fatal acidosis or alkalosis, particularly in 
chronic overmedication for long-term treatment. 
For this reason, patients given lithium treatment 
should have frequent blood checks to make sure 
a toxic level has not been reached. Lithium is not 
recommended for those who have kidney or heart 
disease or for women in early or late pregnancy. 

It should not be taken with alcohol (combina- 
tion can result in lithium poisoning); combination 
with caffeine reduces lithium's effect, and combi- 
nation with cocaine can cause psychosis. In addi- 
tion, lithium in combination with a wide range of 
drugs can cause a variety of problems, including 
increased toxicity, hypothermia, major seizures, 
and sedation. 

Poisonous part 

It is not clear how lithium produces toxic effects, 
but the drug seems to focus primarily on the kid- 



neys. Lithium is thought to stabilize cell metabo- 
lism; in large amounts it depresses neural function, 
but entry into the brain is slow. This explains the 
delay between peak blood levels and central ner- 
vous system effects after acute overdose. 

Symptoms 

Within 1 5 minutes to an hour after ingestion of an 
excessive dose, tremors appear, followed by twitch- 
ing, apathy, speech problems, appetite loss, hair 
loss, dry mouth, seizures, blurred vision, confusion, 
coma, and death. After acute ingestion, victims 
experience mild nausea and vomiting, but these 
are delayed for several hours. Patients with long- 
term intoxication have more serious symptoms; 
toxicity may be severe with levels only slightly 
above recommended doses. 

Treatment 

There is no specific antidote. Stop administering 
lithium and give sodium chloride intravenously. 
In cases of ingestion of acute large doses, perform 
gastric lavage and administer activated charcoal 
followed by a saline cathartic. Drink plenty of flu- 
ids; dialysis may be required. Potassium may be 
given as well. 

loquat (Eriobotrya japonica) [Other names: Japa- 
nese medlar, Japanese plum.] This small ever- 
green tree is cultivated in Cahfornia, Florida, the 
Gulf coast states, Hawaii, and the West Indies. It 
has large, stiff leaves and fragrant white flower 
clusters; the fruit is yellow and shaped like a pear. 

Poisonous part 

While the unbroken seed is harmless, the pit kernel 
is toxic and contains cyanogenic glycosides that 
release hydrocyanic acid upon interaction with 
water in the gastrointestinal tract. 

Symptoms 

Since the glycosides must be broken down before 
the hydrocyanic acid is released, some hours may 
pass before symptoms appear. When they do, they 
include abdominal pain, vomiting, sweating, and 
lethargy. In severe poisoning cases, there may be 
convulsions and coma. 



144 lorchel 



Treatment 

If conscious, victims may be given gastric lavage 
followed by a 25 percent solution of sodium thio- 
sulfate distilled into the stomach; activated char- 
coal absorbs cyanide but releases it slowly during 
passage through the intestine. In those who are 
losing consciousness, treat shock, correct acido- 
sis, and give respiratory assistance with oxygen, 
together with the administration of a cyanide 
antidote. 

See also cyanogenic glycosides. 



lorchel See turbantop. 



LSD (lysergic acid diethylamide) [Other names: 
acid, blotter acid, haze, microdots, purple haze, 
sunshine, window panes.] LSD is a synthetic hal- 
lucinogenic drug that was the drug of choice dur- 
ing the 1960s. A synthetic derivative of ergot, it is 
usually in the form of a clear liquid, and it can be 
either injected or ingested (often in a soaked sugar 
cube). Its distribution and manufacture are gov- 
erned by the Controlled Substances Act because of 
its potential for abuse. 

Symptoms 

Although its mechanism is not yet clear, LSD 
affects the brain and produces hallucinations, 
hyperexcitability, tremors, prolonged mental dis- 
sociation, psychopathic personality disorders, con- 
vulsions, and coma, with a possible risk of suicide. 
There have been reports of numerous "flashbacks" 
many years after the final dose has been taken. 
Symptoms can appear within 20 minutes of inges- 
tion, but there is no set toxic dose, since effects 
vary widely from one person to another depend- 
ing on the situation and the person's current emo- 
tional state. However, hallucinations and visual 
illusions are dose related; the toxic dose may be 
only slightly greater than the dose required to 
produce hallucinations. 



Treatment 

There is no specific antidote, although Valium can 
control the hyperactivity or convulsions; coma is 
treated in the same way as barbiturate poisoning. 
Do not induce vomiting, since it is not effective and 
can worsen psychological distress; gastric lavage 
should be performed only if a massive dose has 
been ingested within 30 to 60 minutes. Administer 
activated charcoal. 

See also barbiturates; ergot. 

lye The common name for sodium hydroxide and 
one of a wide variety of caustic alkalies found in 
drain cleaners, oven cleaners, and other household 
products, this is one of the most dangerous house- 
hold poisons. Toddlers in particular are vulnerable 
to accidents, including burns to the eye, skin, and 
esophagus. Because of the dangers of ingestion of 
lye in particular, federal legislation has required 
safety caps on containers of more than 2 percent 
concentrations of lye and banned use of more than 
10 percent sodium hydroxide in household liquid 
drain cleaners. 

Symptoms 

In small doses, lye causes nausea, vomiting, cough- 
ing, and the spitting of blood. Larger amounts can 
result in weakness, dizziness, slow, shallow breath- 
ing, and unconsciousness followed by convulsions 
and, sometimes, mild heart attack. Death is almost 
always a result of pulmonary problems. Inhalation 
causes lung damage. 

Treatment 

Gastric lavage only when preceded by endotracheal 
tube in comatose victims. Do not induce vomiting. 
Magnesium or sodium sulfate or citrate may be 
used as a cathartic. Oxygen and supportive therapy 
may also be needed. 

See also alkaline corrosives. 

lysergic acid diethylamide See LSD. 



M 



malathion This is an insecticide generally consid- 
ered to be safe for use around people and animals 
to eliminate pests such as fruit flies, mosquitoes, 
and boll weevils, in addition to household flies and 
lice on farm animals. Malathion is a colorless liquid 
with a definite smell, slightly soluble in water and 
sold as wettable powders, emulsifiable concentrates, 
dusts, or aerosols. While it is possible to become sick 
after skin contamination or inhalation, fatal cases 
have been reported usually only after ingestion. If 
heated, malathion becomes extremely dangerous, 
emitting toxic phosphorous oxide fumes; the addi- 
tion of water transforms this into phosphoric acid. 

In addition, recent research has discovered that 
low doses of malathion can cause a response in 
mice similar to an allergic reaction. These studies 
were begun following reports of rashes and allergy 
symptoms in humans after aerial spraying of mala- 
thion, particularly following medfly spraying in 
the San Fernando Valley in southern California. 
Although scientists at the University of Southern 
California at Los Angeles say the effects of the 
pesticide are probably not life threatening, they are 
unsure how the chemical would affect those with 
impaired immune systems. 

Symptoms 

Almost immediately to within several hours, symp- 
toms begin: dermatitis, headache, nosebleeds, nausea, 
vomiting, diarrhea, blurred vision, excess salivation, 
bronchitis, shock, heart rhythm disturbances, or skin 
irritation; death is caused by the muscle weakness 
that affects the lungs, interfering with breathing. 

Treatment 

Respiratory support must be maintained to guard 
against respiratory failure. 

See also insecticides; organophosphate 

INSECTICIDES. 



mambas The black mamba (Dendroaspis polylepis) 
is one of the most dangerous of all snakes; a large 
black mamba can produce enough venom to kill 10 
adults. Growing up to 14 feet, its color ranges from 
dull gray to greenish brown or black, depending 
on its age. This highly aggressive snake is found in 
savannas, rocky outcrops, thickets, and remnant 
forests in Ethiopia, Somalia, and Southwest Africa. 
Extremely agile and speedy, it is the most territo- 
rial of all the mambas; when cornered, it rears up 
to strike, biting a person's head or trunk. Its potent 
venom is neurotoxic and cardiotoxic; the fatality 
rate is nearly 100 percent without antivenin. 

The green mamba (D. angusticeps) is smaller and 
less aggressive and prefers to live in trees. Highly 
agile, this snake is found in forests and thickets and 
is highly dangerous when restrained. 

The mambas have no upper jaw teeth behind 
their two fangs and are not aggressive unless pro- 
voked or restrained. Their color often conceals 
them until an unwary intruder gets too close. 

Symptoms 

Local pain, swelling, paralysis of vocal cords, sweat- 
ing, vomiting, restlessness, drowsiness, collapse, 
coma, and death. 

Treatment 

Antivenin is available. 

See also antivenin; snakes, poisonous. 

mandrake, American [Other names: devil's apple, 
hog apple, Indian apple, raccoon berry, umbrella 
leaf, wild jalap, wild lemon.] Also known as the 
mayapple (Podophyllum pelatiim), this plant pro- 
duces fruit that, when ripe, can be eaten safely in 
moderation even by children. Eating the plant is 
fatal within 30 minutes. 



145 



146 manganese 



The Middle Eastern variety was a famous love 
potion during the Middle Ages, when it was 
also considered to have magical properties. Some 
believed it would protect against evil spirits, and 
others believed that elves could not tolerate its 
smell. The ancient Greeks associated the mandrake 
with Circe, the witch. Because it was believed that 
touching the root would be fatal, dogs were trained 
to pull the dark brown root out of the ground, 
whereupon, according to legend, the root would 
shriek and the dog would die. Others believed that, 
pulled from the ground while muttering the correct 
incantation, the plant could bring forth the devil. In 
fact, the simple possession of mandrake could mark 
the owner as a witch, and three German women 
were executed in 1630 for just such a crime. 

The American mandrake grows in moist woods 
and pastures. Found from Quebec to Florida, west 
to Ontario, Minnesota, and Texas, it grows about 
1-foot tall, with a jointed dark root about half the 
size of a finger, branching in a fork that resembles 
a pair of legs; in fact, it resembles a tiny human 
being. Leaves are deeply lobed with one white 
flower that appears in the spring, resembling a 
strawberry blossom; this is followed by a yellow 
fruit that is edible when ripe (and is sometimes 
used for preserves). 

Poisonous part 

Rootstock, stem, flower, leaves, and unripe fruit 
contain several hallucinogenic alkaloids, including 
hyoscyamine (atropine) and mandragorin; toxins 
also include podophylloresin and its glucoside, and 
alpha- and beta-peltatin. When green, the rhi- 
zome, foliage, seeds, and green fruit are poisonous. 
Herbahsts believe the best time for collecting the 
root is the latter part of October or early November, 
after the fruit is ripe. 

Symptoms 

Within a few minutes to a half hour after ingestion 
of large amounts of the plant or topical application 
of the resin, mandrake poisoning causes severe 
diarrhea and vomiting, sedation, slowed heart rate, 
pupil dilation, coma, and death. The mandrake's 
close relative, the mayapple, causes gastroenteritis, 
headache, and collapse and, when combined with 
alcohol, can be fatal within 14 hours. 



Treatment 

There is no specific antidote; give fluid replacement 
and blood transfusions if necessary. 

manganese Workers in mining, metalworking, 
foundry, and welding occupations are generally the 
only people exposed to manganese toxicity from 
chronic rather than acute exposure. 

Poisonous part 

While the exact mechanism of manganese toxicity 
is not known, inhalation affects the central ner- 
vous system; manganese is not well absorbed from 
the gastrointestinal tract. 

Symptoms 

Although an acute intoxication is possible, causing 
pneumonitis, it is more likely that workers would 
be poisoned as a result of chronic exposure to low 
levels of manganese over a period of months or 
years. In the case of chronic exposure, manganese 
causes an affective psychiatric disorder (often mis- 
diagnosed as schizophrenia or psychosis). This is 
followed by further signs of brain disease, such as 
parkinsonism or similar movement disorders. 

Treatment 

For cases of acute inhalation toxicity, administer 
oxygen and treat symptoms. Long-term exposure 
should be treated with the typical drugs for psy- 
chiatric and movement disorders. Chelating agents 
have not been proven effective once chronic brain 
damage has occurred. 

massasauga (Sistrurus catenatus) One of three 
rattlesnakes from the family Viperidae, this pygmy 
rattler ranges from the Great Lakes southwest to 
southeastern Arizona and Mexico. Its name, which 
is from the Chippewa language, means "great river 
mouth" and is thought to indicate the snake's habi- 
tat in the land of the Chippewa — swamps around 
rivers. 

The massasauga has a stocky tail with a small 
rattle, and rounded dark blotches on its back and 
sides. A light-bordered dark bar runs from the 
eye to the rear of its jaw. The snake may grow to 



meclofenamate 147 



40 inches. This "swamp rattler" is found in bogs, 
swamps, marshes, floodplains, and dry woods 
in the East; grassy wetlands, rocky hillsides, and 
the sagebrush and desert grasslands of the West. 
Unlike many snakes, massasaugas do not hiber- 
nate communally in an upland den but sleep 
alone in a mammal or crayfish burrow. They 
emerge in spring in response to the rains and ris- 
ing water. 

While fairly poisonous snakes, they are not 
aggressive and normally bite only when disturbed. 

Symptoms 

Symptoms appear within 15 minutes and include 
excessive thirst, nausea, vomiting, shock, paralysis, 
respiratory problems, anemia, kidney problems, 
and sometimes death. The bite of a rattlesnake is 
painful. Indications of a serious bite include swell- 
ing above the elbows or knees within two hours, 
hemorrhages, numbness at the puncture site, tin- 
ghng around the mouth, yellow vision, vomiting, 
and violent spasms. 

Treatment 

Antivenin is available. 

See also pit viper; rattlesnake, canebrake; 
rattlesnake, cascabel; rattlesnake, eastern dia- 
mondback; rattlesnake, Mexican west coast; 

RATTLESNAKE, RED DIAMONDBACK; RATTLESNAKES; 
RATTLESNAKE, TIMBER; RATTLESNAKE, WESTERN DIA- 
MONDBACK; sidewinder; viper, Gaboon; viper, 
JUMPING; viper, Malayan pit; viper, Russell's; 

VIPERS; VIPER, SAWSCALE; viper WAGLER'S pit; WATER 

moccasin; wutu. 

matches Serious cases of poisoning from ingest- 
ing matches are quite rare since the principal 
component of white or yellow phosphorus was 
replaced by red or by phosphorus sesquisulfide. 
The "strike anywhere" type of match is made of 
a nonpoisonous paste containing 6 percent phos- 
phorus sesquisulfide and 24 percent potassium 
chlorate, plus zinc oxide, red ochre powdered 
glass, glue, and water. "Safety" (or strike-on-box) 
matches are nonpoisonous; their chief ingredient 
is potassium chlorate. Book matches are similar to 
the safety type of match. 



Accidental ingestion of matches by children 
often occurs, but it produces relatively insignificant 
side effects. Even if a child ate an entire book of 20 
match heads, the total amount of potassium chlo- 
rate is still only 1/20 of the toxic dose. 

meadow saffron (Colchicum autumnale, C. spe- 
ciosum, C. vernum) [Other names: autumn crocus, 
fall crocus, naked ladies.] This crocus look-alike 
and ancient abortifacient is a member of the lily 
family and is often mistaken for an onion. It 
has long, tubular purple or white flowers that 
emerge from an underground bulb. Highly toxic, 
it is found in damp and woodsy areas in England, 
Wales, and Scotland. Goats, which are immune 
to the poison, can eat the plant and pass on the 
poison in their milk, which will sicken anyone 
who drinks it. 

Poisonous part 

All parts (especially the bulbs) are toxic; tincture of 
colchicine is made from the seeds of C. autumnale, 
and the drug colchicine is used as a rheumatic. 

Symptoms 

Within two to six hours after ingestion, the victim 
begins to exhibit some symptoms similar to those 
of arsenic poisoning: burning throat, intense thirst, 
vomiting, difficulty in swallowing, bloody diarrhea, 
stomach pain, sensory disturbances, muscle weak- 
ness, delirium, and heart and breathing failure. 
Meadow saffron poisoning is fatal in half of all 
cases, although it may not occur until three days 
after ingestion. 

It is also possible to suffer chronic colchicine poi- 
soning, with symptoms of hair loss and blood and 
protein in the urine and colchicine in the feces. 

Treatment 

Because colchicine is only slowly excreted, the 
victim is often ill for a long time. Painkillers and 
atropine may be given to alleviate stomach pain 
and diarrhea; fluids are required. 

meclofenamate See nonsteroidal anti- 
inflammatory DRUGS. 



148 meperidine 



meperidine (Demerol) Introduced in 1939 as a 
means of reducing the pain associated with muscle 
spasms, this drug was later found to have many 
other painkilling abilities. It soon became almost 
as popular a drug as morphine, but it is only 
about one-tenth as potent. Still, meperidine is a 
fairly strong analgesic and is used for treatment of 
moderate to severe pain, to supplement anesthesia 
before an operation and to relieve the pain of labor 
during childbirth. 

Symptoms 

Large doses of meperidine can cause twitches, 
tremors and convulsions, and the drug is especially 
dangerous when mixed with monoamine oxidase 
(MAO) inhibitors (a class of antidepressants). In 
fact, if it is taken within two weeks of an MAO 
inhibitor, it can cause symptoms similar to those 
in acute narcotic overdose (including convulsions, 
high blood pressure, coma, and death). 

Treatment 

Medical help should be sought immediately. Stimu- 
lants such as strong tea and coffee will help to keep 
the victim awake. If the victim is discovered soon 
after ingestion and is conscious, induce vomiting. 

mercury Every known form of this highly toxic, 
silvery liquid metal is poisonous, and since there 
are more than 115 known mercury compounds, 
there are many opportunities for mercuric poi- 
soning to occur. It is widely used in skin and hair 
bleach, dusting or wettable powders and fumi- 
gants, cathartics, antiseptics and diuretics, and in 
explosives, tooth fillings, electrical lamps, batteries, 
paints, and felt. In the past, many milhners used 
mercury to help shape hats; it has been suggested 
that Lewis Carroll's Mad Hatter may really have 
been suffering from mercury poisoning, as did 
many hatters of the 1800s. 

Its toxicity depends on the chemical form in 
which it appears, and in its most common form, 
as a free metal in fever thermometers, mercury 
is not a serious threat if ingested, since it is not 
well absorbed by the body. However, breathing 
mercury vapor is more hazardous. Employees in 
dental offices may also be exposed to excess levels 



of mercury, via recirculation ventilation systems or 
sloppy conditions. Mercury chloride found in anti- 
septics is the most toxic of all mercury compounds. 
Organic mercurials that are used to treat seeds are 
highly toxic, and acute cases of poisoning have 
been reported from fish contamination or water 
pollution. 

There is a large number of professions whose 
workers are exposed to mercury, including those 
who make barometers, batteries, boilers, calibration 
instruments, caustic soda, carbon brushes, ceram- 
ics, chlorine, dental amalgam, electrical apparatus, 
neon fights, pressure gauges, disinfectants, dyes, 
explosives, fireworks, inks, drugs, insecticides and 
pesticides, and wood preservatives. 

Symptoms 

Acute poisoning from inhaling mercury vapor 
occurs almost immediately, causing stomach prob- 
lems, coughing, fever, nausea, vomiting, and diar- 
rhea. The vapor affects the brain and lungs, 
attacking the respiratory system and causing pneu- 
monia, pulmonary edema, and ventricular fibrilla- 
tion followed by death. Chronic poisoning results 
in damage to the central nervous system and can 
cause psychosis. Ingestion of mercuric chloride 
and other soluble mercuric salts can cause thirst, 
abdominal pain, vomiting and diarrhea, followed 
by kidney damage, and death. Skin contamination 
with mercury compounds causes a variety of symp- 
toms, including depression, sleeplessness, weight 
loss and anorexia, headaches, anxiety, hallucina- 
tions, loose teeth, and tremors. 

Treatment 

Dimercaprol and treatment of symptoms. 

See also fish contamination; mercury and den- 
tal FILLINGS. 

mercury and dental fillings For decades, experts 
in the field of toxicology were sharply divided over 
whether mercury contained in dental fillings posed 
a hazard to human health. In a study published in 
2006, for example, 465 patients with chronic mer- 
cury toxicity reported severe fatigue (32.3 percent), 
memory loss (88.8 percent), and depression (27.5 
percent). When amalgam mercury fillings were 



methyl alcohol 149 



removed and appropriate treatment was adminis- 
tered, patients experienced a significant reduction 
in symptoms to a level reported by healthy sub- 
jects. Yet other experts, including those at the Food 
and Drug Administration (FDA) and the National 
Institutes of Health, for many years insisted that 
amalgams were at least as safe as the available 
alternatives. 

Then in June 2008, the FDA announced that 
"dental amalgams contain mercury, which may 
have neurotoxic effects on the nervous systems 
of developing children and fetuses." It also added 
that when amalgam fillings are "placed in teeth 
or removed they release mercury vapor," and that 
this effect also occurs when people chew. The FDA 
has decided to review its rules about amalgams 
and may alter its position on the use of mercury 
in fillings. 

See also mercury; fish contamination. 

metal cleaner See alkaline corroslves. 



metaldehyde This is a type of inorganic chemical 
insecticide often used in combination with calcium 
arsenate and used to control slugs and snails. It is 
also sold as fuel for small heaters that can cause 
toxic vapors if not properly ventilated. Poison 
control centers report incidences of children being 
poisoned after mistakenly eating slug or snail bait 
or heater fuel tablets. 

Ingestion of 100 to 150 milligrams per kilogram 
may cause convulsions, and ingestion of more than 
400 mg/kg is potentially lethal. 

Symptoms 

Metaldehyde is a stomach irritant; between one 
and three horns after ingestion it causes nausea, 
vomiting, stomach pain, flushed face, fever, mus- 
cular rigidity, and twitching. In severe poisonings, 
convulsions and coma are followed by death from 
respiratory failure. Liver and kidney damage have 
been reported. 

Treatment 

There is no specific antidote. Perform gastric lavage 
immediately after ingestion, followed by activated 



charcoal and cathartics, with supportive therapy 
including plenty of fluids. Do NOT induce vomit- 
ing. Demulcents (such as milk) may reheve gastric 
distress; sedation may also be required. 
See also inorganic chemical insecticides. 



methanol See methyl alcohol. 



methocarbamol This centrally acting muscle 
relaxant is used in the control of painful muscle 
spasms following the bite of the black widow spider 
and strychnine poisoning. Onset of action almost 
immediately follows intravenous administration. 
See also black widow spider; strychnine. 

methyl alcohol (wood alcohol) Also known 
as methanol, this common household solvent is 
related to ethyl alcohol and is found in solvents, 
perfumes, windshield washing liquids, duplicating 
fluid, antifreeze, shellac, and paint removers. 

It is far more poisonous than the ethyl alcohol 
found in cocktails, because it metabolizes into 
formaldehyde upon ingestion; it also takes far 
longer to eliminate methyl alcohol from the body. 
While it can produce intoxication, its metabolic 
products may cause metabolic acidosis, blindness, 
and death. 

Methyl alcohol is a liquid at room temperature, 
evaporates quickly and can be swallowed, inhaled 
as a vapor or absorbed through the skin. In the 
past, moonshine makers (who distill ethyl alco- 
hol from fermented grain) sometimes mistakenly 
mixed wood shavings in with the brew, resulting 
in a toxic brand of moonshine. (Methyl alcohol is 
made from fermented wood.) 

Symptoms 

The fatal oral dose of methyl alcohol is estimated 
to be 30 to 240 milliliters. Because methyl alcohol 
metabohzes slowly in the body, there is a latency 
period ranging from 12 to 48 hours between inges- 
tion/inhalation and symptoms. In the first hours 
after ingestion, the primary symptom is intoxica- 
tion because the body has not yet begun to break 
down the substance into more toxic products. Once 



150 methyl bromide 



methyl alcohol is transformed into formaldehyde 
in the body, it causes fatigue, headache, nausea 
and vomiting, vertigo, back pain, severe abdominal 
pain, vision problems, dizziness, and blindness. 
(These symptoms will appear even later if ethanol 
has been drunk at the same time.) In large doses, 
symptoms progress to rapid, shallow breathing, 
cyanosis, coma, precipitous drop in blood pressure, 
and death from respiratory arrest. An autopsy 
would show massive organ damage, especially in 
the eyes. Breathing fumes can cause headache, eye 
irritation, dizziness, visual disturbances, and nau- 
sea. In extreme cases, inhaling these fumes can be 
fatal; it damages the liver, heart, kidneys, and the 
lungs, predisposing them to pneumonia. 

Treatment 

Ethanol (100 proof) is administered to interfere 
with the metabolism of methyl alcohol; within two 
hours of ingestion, gastric lavage is preferred, but 
syrup of ipecac may be given at home to induce 
vomiting before medical help arrives. Ethanol is 
then administered orally or intravenously for the 
next four days until the methyl alcohol is excreted; 
kidney dialysis may also remove the alcohol from 
the blood. Folic acid may also be administered; 
and 4-methylpyrazole (fomepizole) can inhibit 
alcohol dehydrogenase and prevent methyl alco- 
hol metabolism. Activated charcoal has not been 
shown to absorb methyl alcohol efficiently, and it 
may also delay the absorption of orally adminis- 
tered ethanol. 



methyl bromide This odorless, colorless gas is 
used in insecticidal fumigants and fire extinguish- 
ers and in the production of chemicals and dyes. It 
is considered to be a potential industrial carcinogen 
by the National Institute of Occupational Safety 
and Health (NIOSH). It can be inhaled or absorbed 
easily through the skin; methyl bromide also easily 
penetrates protective clothing and can be retained 
in boots and clothing for some time. 

Symptoms 

Methyl bromide affects the central nervous system, 
the respiratory tract, the skin and the cardiovas- 
cular system. There is a wide variance in onset of 



symptoms, ranging from a few minutes to two days 
after ingestion. Methyl bromide irritates the eyes, 
skin, and upper respiratory tract, which may lead to 
pulmonary edema; skin contamination can cause a 
rash or chemical burns. With acute exposure, there 
may be malaise, vision disturbances, headache, 
nausea, vomiting, vertigo, tremor, seizures, and 
coma followed by death from pulmonary or circu- 
latory failure. In addition, chronic exposure may 
lead to dementia or psychosis. 

Treatment 

Some scientists recommend the use of dimercaprol 
or acetylcysteine, although their use has not been 
tested in controlled studies. Remove all contami- 
nated clothing and wash the skin with soap and 
water; irrigate eyes with saline or tepid water. 
See also ethyl alcohol. 



methyl chloroform See trichloroethane. 

methylene chloride One of a group of chlori- 
nated hydrocarbons, this chemical solvent is listed 
as a human carcinogen by the National Toxicology 
Program of the U.S. Department of Health and 
Human Services. It is encountered by millions of 
Americans every day in products ranging from 
paint strippers and thinners to paint, hair spray, 
antiperspirants, room deodorants, and Christmas 
tree hght sets. Upon combustion, it can produce 
phosgene, chlorine or hydrogen chloride; it was 
considered to be one of the least toxic of the chlo- 
rinated hydrocarbons, but now it is a suspected 
carcinogen. 

Methylene chloride irritates mucous membranes 
and depresses the central nervous system. Carbon 
monoxide is generated within the body during 
metabohsm of methylene chloride. 

Symptoms 

Inhalation is the most common route of intoxi- 
cation and causes skin irritation, nausea, vomit- 
ing, and headache. Severe exposure may lead to 
pulmonary edema, heart problems, and central 
nervous system depression with respiratory arrest. 
Ingestion can lead to corrosive injury and system 



Mexican hallucinogenic mushroom 151 



intoxication. Chronic exposure is toxic to bone 
marrow, the kidneys, and the liver. 

Treatment 

Administer 100 percent oxygen by tight-fitting 
mask or endotracheal tube; if skin or eyes are con- 
taminated, wash thoroughly. In case of ingestion, 
do NOT induce vomiting, perform gastric lavage 
if the victim has ingested within the past 30 to 60 
minutes or has ingested a large amount. Adminis- 
ter activated charcoal and a cathartic, although the 
effectiveness of the former is not known. 

See also chlorinated hydrocarbon pesticides. 



methylenedioxymethamphetamine (MDMA) See 

ECSTASY. 



methyl phenidate See Ritalin. 

methyl mercury See fish contamination; 

MERCURY. 

metoclopramide This antinausea drug is used to 
control persistent nausea and vomiting often found 
in poisoning cases, especially when activated char- 
coal may not be given. 

Mexican beaded lizard (Heloderma horridum) 

One of only two poisonous lizards in the world 
out of more than 3,000 lizard species, the Mexican 
beaded lizard is found only in Mexico and is a rela- 
tive of the Gila monster, also a member of the Helo- 
derma genus. Slightly larger than the Gila monster, 
the Mexican beaded lizard is still not a very large 
animal — between 19 and 29 inches long; it is a 
mixture of black, yellow, and pink and has knobby 
scales. Both lizards are sluggish but have a strong 
bite. Fatalities from the bite of a Mexican beaded 
lizard are rare. 

Beaded lizards are nocturnal and mate during 
summer, laying between three and five eggs in 
autumn and winter. Although these lizards are 
relatively slow moving, they can bite quickly and 



hang on stubbornly. While biting, they chew so 
that the grooved teeth can allow the venom to 
flow from the glands at the base of the mouth. In 
general, the bite of the beaded lizard is not fatal, 
but it is quite painful. There have been only eight 
recorded deaths from bites of both these hzards. 

Beaded lizards live underground, either in aban- 
doned holes or ones they dig themselves, they 
locate their food by scent rather than sight, follow- 
ing a trail in much the same way as a bloodhound 
does. 

See also Gila monster. 



Mexican hallucinogenic mushroom (Psilocybe 

mexicana) Also known as "magic mushrooms," 
these are a species of mushrooms that contain 
the hallucinogenic substance psilocin-psilocybin, 
which American Indians have used for thousands 
of years in their religious ceremonies. 

The Psilocybe genus includes more than 100 
different species of the little brown mushrooms, 
which are found growing in grass and manure 
heaps — especially after spring rains. Though found 
primarily in the South, they grow almost every- 
where in the United States. One of the easiest 
ways to identify the Psilocybe mushroom is by its 
blue-green discoloration in areas where it has been 
handled or damaged. 

Symptoms 

Within an hour of ingestion, its effects — which are 
usually considered pleasant — appear: euphoria, 
loss of sense of distance and size, and hallucina- 
tions. Symptoms will last between four and six 
hours depending on the quantity of toxin ingested, 
the mood and personality of the person and the 
setting of the experience. Effects lasting longer 
than 24 hours are not due to a natural toxin but to 
the consumption of a mushroom with another hal- 
lucinogen added (usually phencychdine or PGP). 
The mushrooms can cause high fever, convulsions, 
and death in children who have eaten them. 

Treatment 

For those who seek medical assistance, treat- 
ment usually involves reassurance, although seda- 
tion (with diazepam) is sometimes necessary. In 



152 Mexican moccasin 



children, treatment includes external cooling and 
respiratory support; it may be necessary to admin- 
ister diazepam to control convulsions. 

See also hallucinogenic mushrooms; mush- 
room POISONING. 



Mexican moccasin See cantil snake. 



midazolam This ultrashort-acting benzodiaze- 
pine is used to help manage anxiety, agitation, and 
psychosis following overdose of hallucinogenic or 
stimulant drugs such as LSD or amphetamines. It 
is also used to induce sedation and amnesia during 
placement of an endotracheal tube. 

See also amphetamines; benzodiazepines; LSD. 



Minipress (prazosin hydrochloride) One of a 

group of antihypertensives, this toxic medicine 
is available as a white crystalline water-soluble 
capsule. 

Symptoms 

Within 30 to 90 minutes after ingestion, Minipress 
overdose causes headache, drowsiness, hair loss, 
weakness, nausea, vomiting, diarrhea, shortness of 
breath, nervousness, rapid heartbeat, depression, 
rash, itching, blurred vision, loss of consciousness, 
and death. 

Treatment 

Atropine is administered while monitoring the car- 
diorespiratory systems and the kidney function. 
See also antihypertensive drugs. 



mirex This type of synthetic organic insecticide 
is a chlorinated hydrocarbon that is almost impos- 
sible to dissolve in water and is generally no longer 
used as an insecticide. Emergency exceptions for 
specific uses are allowed, however. 

Mirex was used throughout the southeastern 
United States to control fire ants, other ant species, 
and yellow jackets. It breaks down in the soil and 
forms kepone, a chlorinated organic insecticide 
banned from use in 1978. 



Symptoms 

Inhalation, ingestion, or skin contamination can 
cause chest pain, weight loss, rash, and a range of 
neurological problems including tremors, mental 
alterations, weakness, and slurred speech. Both 
mirex and its derivative, kepone, cause cancer in 
experimental animals. 

Treatment 

Gastric lavage followed by saline cathartics. Avoid 
all fats and oils (including milk), since they increase 
the rate of absorption. Administer phenobarbital 
sodium for tremors and barbiturates for convul- 
sions, and provide oxygen if necessary. If the skin 
has come in contact with these insecticides, wash 
with soap and water immediately to head off skin 
problems and systemic absorption. Remove con- 
taminated clothing. 

See also chlorinated hydrocarbon pesticide. 



mistletoe (American: Phoradendron rubrum, P. 
serotinum, P. tomentosum; European: Viscum 
album) This popular winter holiday plant is a par- 
asite of deciduous trees in the southeastern United 
States, and the whole mistletoe plant — especially 
the berries — is poisonous, although seldom fatal. 

Mistletoe has thick, leathery leaves, with white 
translucent berries in the P. serotinum and P. tomen- 
tosum varieties and pink berries in the P. rubrum 
variety. P. serotinum is the variety typically sold as 
a decorative holiday plant at Christmas; it grows 
from New Jersey to Florida and west to southern 
Ilhnois and Texas. P. tomentosum is found from Kan- 
sas to Louisiana and west to Texas and Mexico. 

V. album is a parasite found principally on apple 
trees and, although a European plant, has been 
introduced into Sonoma County, California. Its thick, 
leathery leaves are up to three inches long and yellow- 
green in color; the fruit is a sticky white berry. 

Mistletoe is a plant steeped in legend and mys- 
tery. It is said that mistletoe was once a tree, the 
wood of which had been used to make Christ's 
cross, and was relegated to exist only as a parasite 
ever after. Similarly, it was an herb of the under- 
world in both Greek and Roman legends, while in 
Britain the Druid priests were said to use mistletoe 
in many important religious ceremonies. Tradition 



mold 153 



says that the mistletoe was the "golden bough" that 
the Trojan hero Aeneas, forefather of the Romans, 
carried with him on his descent into Hades. The 
bough opened the gates of hell for the hero and 
brought him safely back. 

Its reputation as an herb of love, in which 
two people standing under it at Christmas must 
kiss, originated in Scandinavia, when Balder (the 
god of peace) was killed with an arrow dipped in 
mistletoe. When his fellow gods asked that his life 
be spared, mistletoe was given to the god of love, 
who announced that anyone who passed beneath 
it must be given a kiss as a symbol of love. It sub- 
sequently became a part of the Christmas celebra- 
tions when the Druids used the greens as a way of 
welcoming the New Year. 

Poisonous part 

Stems, leaves, and berries of this plant contain 
toxic amines and proteins called phoratoxins, toxic 
lectins that inhibit synthesization of proteins in the 
intestinal wall. They can cause hallucinations, slow 
heartbeat, high blood pressure, heart attacks, and 
cardiovascular collapse. While poisoning is rarely 
fatal, there have been cases in which children have 
died after eating mistletoe berries. Tea brewed from 
the berries has also been fatal. 

In the European variety (V. album) only the 
leaves and stems are toxic, containing a toxic lec- 
tin (toxalbumin) called viscumin, which interferes 
with protein synthesis. In addition, related lectins 
called viscotoxins are also found. 

In addition to its own toxic properties, mistletoe 
may also take up poisonous substances from the 
tree on which it lives. 

Symptoms 

Similar to those of poisoning by digitalis, symptoms 
appear after a delay of a few hours and include 
severe nausea, vomiting, diarrhea, stomach cramps, 
difficulty in breathing, slow pulse, dehrium, hallu- 
cinations, and coma. 

In the European variety, poisoning symptoms 
are similar to, but less toxic than, those caused by 
the lectins in rosary pea (Abrus prevatorius) and cas- 
tor bean (Ricinus communis). Symptoms in this vari- 
ety appear some time after ingestion and include 
abdominal pain and diarrhea together with lesions 



of the intestinal tract. Severe poisoning with this 
variety of mistletoe is rare. 

Treatment 

Treat as for severe gastroenteritis, with replace- 
ment of fluids and electrolytes. 

mold The exact number of species of mold is 
unknown, but it is estimated to be as many 
as 300,000 or more. Molds are fungi that can 
grow and develop indoors and outdoors and can 
be found in virtually every environment, year 
round. Although they grow best in damp, warm, 
humid conditions, they spread and reproduce 
spores, which can survive harsh environments and 
become active again when conditions are favor- 
able. Indoors, those environments are generally 
basements, showers, or damp attics, where humid- 
ity levels are high; outdoors, they can be found 
in damp, shady areas or places were vegetation is 
decomposing. Some molds are cryophytes (which 
can adapt to low temperatures), some are thermo 
tolerant (they can adapt to a wide range of tem- 
peratures), and some are thermophiles (they adapt 
to high temperatures). Depending on the species, 
these molds will grow in nearly any environment. 
Temperatures in excess of 500 degrees Fahrenheit 
have not been able to destroy some molds, includ- 
ing the toxic Stachybotrys (see below). 

Some people are sensitive to molds, and their 
reactions can range from mild nasal stuffiness and 
wheezing to severe reactions such as fever and 
shortness of breath. Individuals who have chronic 
lung conditions may develop mold infections in 
their lungs. The term "toxic mold" is somewhat mis- 
leading: while the molds themselves are not toxic, 
certain types produce secondary metabolites that 
produce mycotoxins. When susceptible individuals 
breathe in mold spores and mycotoxins they can 
become ill. Mold and mycotoxins are implicated in 
some cases of sick building syndrome. 

The molds most commonly found both indoors 
and outdoors throughout the United States are 
Alternaria and Cladosporium; others that are often 
seen are Aspergillus, Penicillium, Helminthosporium, 
Epicoccum, Fusarium, Mucor, Rhizopus, and Aureo- 
basidium. One of the mycotoxins, aflatoxin, is 



154 monkshood 



produced by Penidllium, Aspergillus flavor, and Asper- 
gillus parasiticus. Four different aff atoxins have been 
identified (Bl, B2, Gl, and G2), with Bl being the 
most toxic, carcinogenic, and prevalent. 

Much less common but significantly dangerous 
are the molds Stachybotrys chartarum and Chae- 
tomium, which have been proven to produce 
mycotoxins that can lead to autoimmune disease. 
Strachybotrys grows on cellulose products (e.g., 
wood, paper, insulation, fiberboard, hay, straw) 
that has gotten wet. This mold can be found in 
homes and other buildings that have been in 
floods, basements or attics that have been exposed 
to water, and barns and other outbuildings. 

Symptoms 

Nasal and throat irritation, cough, shortness of 
breath, chronic bronchitis, learning disabilities, 
mental deficiencies, heart problems, cancer, mul- 
tiple chemical sensitivity, rash, and diarrhea are 
all possible symptoms associated with exposure to 
mold. Animal studies suggest that Chaetomium spe- 
cies may cause autoimmune disorders (e.g., rheu- 
matoid arthritis, chronic fatigue syndrome, lupus) 
but no scientific studies in humans have been done. 
Exposure to the mycotoxins of the more dangerous 
molds may include nasal infections, peritonitis, and 
cutaneous lesions. 

Treatment 

Symptomatic for the signs and symptoms of mold 
exposure. The best "treatment" is to remove the 
mold and its source. If the affected area is large, 
professional mold removal service may be required. 
For smaller areas, a nonammonia soap or detergent 
in hot water should be used to scrub the affected 
area with a stiff brush or cleaning pad. Rinse the 
area with water and then disinfect the area with a 
solution of household bleach (one-half cup of bleach 
per gallon of water) . Allow the area to dry naturally, 
which allows the bleach to kill all the mold. 
See also sicic building syndrome. 



monkshood (Aconitum) [Other names: aconite, 
bear's foot, friar's cap, helmet flower, soldier's cap, 
western monkshood (A. columbianum), wild monks- 
hood (A. uncinatum), wolfsbane, yellow monks- 
hood (A. lutescens).] Dubbed "queen mother of 



poisons" before the birth of Christ, this extremely 
poisonous plant may reach 6 feet in height with 
small blue, pink, or white flowers and a unique 
hood-shaped upper petal appearing from June to 
September. According to legend, it is ruled by Hec- 
ate, goddess of the underworld, who supposedly 
poisoned her father with it. 

Monkshood is a strikingly beautiful plant rich 
in myth and medicine, history and magic. Often 
grown as an ornamental perennial in shady borders 
around older homes, this plant has flowers that 
resemble delphiniums; the flowers are arranged on 
stems of equal height and distance from each other 
and blossom in an orderly fashion from stem base 
to tip. Although the plant is a perennial, the spongy 
root is an annual and sprouts tiny side roots, each 
capable of producing another monkshood plant. 
Together with larkspur and columbine, monks- 
hood belongs to the buttercup family and includes 
about 100 species in the genus Aconitum. 

The name may come from the Greek akonitos, 
"without struggle" or "without dust," or from the 
Greek city Acona, where a naturalist in the third 
century once identified the plant. Other sources 
suggest the name comes from the hill of Aconitus, 
where Hercules fought with Cerberus, the three- 
headed dog who guards the entrance to Hades. 
Saliva from this dreaded dog's mouth dripped onto 
monkshood, making it a deadly poison. 

In mythology, monkshood formed the cup 
that Medea prepared for Theseus. In Rome, Nero 
ascended to the throne after poisoning Claudius by 
tickling his throat with a feather dipped in monks- 
hood. While it is named for the shape of its flower, 
it was also associated with political intrigue among 
the ranks of the Roman Catholic clergy. Traditions 
holds that Romeo (of Shakespeare's Romeo and 
Juliet) committed suicide with monkshood. 

Witches also made wide use of this plant in 
herbal preparations to induce supernatural experi- 
ences, combining it with belladonna in ointments 
the witches rubbed on their bodies to help them 
"fly." In fact, these two plants produce an irregu- 
lar heart action and dehrium, which is beheved to 
have caused the sensation of flying. During the 
Middle Ages, the plant was widely feared because it 
was thought witches used it to summon the devil. 
In Shakespeare's Macbeth, the witches' brew calling 
for "tooth of wolf" refers to monkshood, which is 



monoamine oxidase (MAO) inhibitors 155 



also known as wolfsbane because arrows dipped 
in the poison kill wolves. (For this same reason, 
medieval folks believed monkshood would protect 
them against werewolves). 

Monkshood thrives naturally and is also cul- 
tivated as a decorative plant in Canada and the 
northern United States, including Alaska. Until 
the 1930s, monkshood was used as a painkiller, 
diuretic, and diaphoretic. Ointments containing 
monkshood have been used externally to treat 
rheumatism, neuralgia, and lumbago, and a tinc- 
ture was used to lower pulse rate and fevers and 
treat cardiac failure. Because of its toxicity, monks- 
hood is rarely used today in medicine, although it 
is still valued in homeopathy as an ointment for 
muscle and joint pain. 

Poisonous part 
The entire plant is poisonous. However, the roots 
and leaves contain the greatest concentration of 
the toxin aconitine and similar alkaloids, including 
picratonitine, aconine, benzoylamine, and neopel- 
line. The alkaloids first stimulate and then depress 
the central and peripheral nerves. One teaspoonful 
of the root is lethal to an adult, and even handhng 
the plant is dangerous to highly sensitive people. 
Because of the root's similarity to Jerusalem arti- 
choke or horseradish, monkshood should never 
be planted near a vegetable garden. Even touching 
the plant's juices to an open wound can cause pain, 
fainting sensations, and suffocation. 

But like many botanical toxins, the one in 
monkshood can be beneficial if administered in 
very small doses. In fact, 18th- and 19th-century 
physicians used monkshood as a cardiac sedative, 
although modern drugs have since replaced it. 

Symptoms 

If monkshood is eaten, symptoms start rap- 
idly with a burning or tingling sensation of the 
lips, tongue, mouth, and throat. Delayed-onset 
symptoms include excessive salivation, nausea, 
vomiting, tightness and numbness in the throat, 
impaired swallowing, and possibly speech impair- 
ment. Intermittent visual disturbances can include 
blurred vision or color patches in the visual field 
and pronounced and prolonged pupil dilation. Diz- 
ziness, prickling skin sensation, muscle weakness, 
and uncoordinated movements can also occur. 



In critical cases there are heart rate and rhythm 
disturbances followed by convulsions and death. 
Death may occur as early as a few minutes after 
ingestion or as late as four days. 

Those who survive report odd hallucinations 
during the poisoning episode and sensory distur- 
bances for a long time afterward. If the victim does 
not die, recovery occurs within 24 hours. 

Treatment 

There is no specific antidote, although gastric 
lavage and oxygen to help breathing, as well as 
drugs to stimulate the heart, may be used. Arrhyth- 
mias should be managed by electrocardiogram 
monitoring. 

See also aconitine. 



monoamine oxidase (MAO) inhibitors A class of 
psychiatric drugs used to treat severe depression 
that also stimulate the central nervous system and 
affect the liver. MAO inhibitors may cause serious 
poisoning either by overdose or through interac- 
tions with other drugs or food. 

For example, eating cheese or drinking alcohol 
(especially red wine) can cause hypertension, 
stroke, and even death. Some MAO inhibitor 
drugs have been taken off the U.S. market because 
of extreme toxicity in combination with other 
drugs. 

MAO inhibitors include furazolidone (Furox- 
one), isocarboxazid (Marplan), nialamide (Niamid), 
pargyhne (Eutonyl), phenelzine (Nardil), procarba- 
zine (Matulane) and tranylcypromine (Parnate). 

Symptoms 

In an acute overdose, symptoms may not appear 
for six to 24 hours, but they should be apparent 
quite soon after eating certain foods or taking 
certain other drugs. Symptoms include anxiety, 
flushing, headache, tremor, sweating, tachycardia, 
and hypertension; severe poisoning causes severe 
high blood pressure, brain hemorrhage, delirium, 
high fever, cardiovascular collapse, and multisys- 
tem failure. 

Treatment 

There is no specific antidote. Treat symptoms; 
monitor temperature and vital signs, with an ECG 



156 monomethylhydrazine 



DRUGS AND FOODS THAT DON'T MIX 
WITH MAO INHIBITORS 

Drug Food 

Amphetamine Beef liver/Beer 

Buspirone Beans 

Dextromethorphan Cheese 

Ephedrine Chicken livers 

Fluoxetine Game meats/Pickled herring 

Cuanethidine Saver Kraut/Snails 

L-Dopa Red wine 

LSD (lysergic acid Yeast 
diethylamide) 

Meperidine (Demerol) 

Metaraminol 

Methyldopa 

Phenylephrine 

Phenylpropanolamine 

Reserpine 

Trazodone 

Tryptophan 



for victims without symptoms. Do not induce 
vomiting because of tfie risk of seizures and 
worsening the high blood pressure; perform gas- 
tric lavage followed by activated charcoal and a 
cathartic. 

See also antidepressants. 



monomethylhydrazine A propellant used in 
rocket fuel, this is also a decomposition product of 
the mushroom toxin gyromitrin and the primary 
toxic component of the gyromitra mushroom. 

Symptoms 

A strong convulsant, this substance can cause cen- 
tral nervous system depression, pulmonary edema 
and cardiovascular collapse, with some kidney 
damage and severe liver damage. 

Treatment 

The antidote is pyridoxine, which may help in the 
control of hyperexcitability and even coma but will 
not protect the liver from damage. 

See also Gyromitra; mushroom poisoning; mush- 
room TOXINS. 



monosodium glutamate (MSG) This natural salt 
is found in low amounts in seaweed, soybeans, 
and sugar beets; refined, it is used to enhance the 
flavor of certain foods (especially red meat, poultry, 
and fish). MSG is commonly used by the processed 
food industry and Asian restaurants as a flavor 
enhancer. The most common processed foods that 
use MSG include meat products, bouillons, pre- 
cooked soups, and gravies in packages, condiments, 
pickles, candy, and baked goods. 

Almost anyone who eats processed food, fast 
food or dines at an Asian restaurant will encounter 
MSG; most of the health complaints have come 
from people eating at Chinese restaurants. Soups 
and foods coated with a liquid sauce often contain 
the highest concentration of MSG, and rice used in 
Japanese sushi also contains high concentrations. 

Labels must indicate which packaged foods 
contain MSG, but avoiding the additive is much 
more difficult in restaurants, since menus usually 
do not mention that the food contains this flavor 
enhancer. Unless it is explicitly stated otherwise, it 
should be assumed that Asian food contains MSG. 

MSG contains the amino acid glutamate, which 
may be responsible for brain damage under cer- 
tain conditions of oxygen deprivation in the brain 
(such as during a stroke), or when ingested in 
large quantities. While the glutamate in MSG is 
considered safe for adults, research at Washington 
University in St. Louis finding that large doses of 
glutamate may damage brain cells prompted the 
Food and Drug Administration to ban MSG from 
baby food in the mid-1970s. 

According to a recent animal study (February 
2008) and several earlier studies, MSG can lead 
to the development of inflammation, obesity, and 
type 2 diabetes. The 2008 study focused on the 
impact of MSG on the liver and found that the sub- 
stance induces obesity and diabetes with steatosis 
(fatty liver) and steatohepatitis (liver inflammation 
caused by fat buildup). These findings caused the 
investigators to suggest that the safety profile for 
MSG be reviewed and that the substance be con- 
sidered for withdrawal from the food supply. 

Symptoms 

Among certain individuals in a subgroup of the 
population, MSG causes "Chinese restaurant syn- 



morphine 157 



drome": tightness in the head and face, headache, 
chest pain, dizziness, sweating, and numbness. 
According to the Food and Drug Administration, 
about 4 percent of the population will have an 
occasional reaction to MSG; about 2 percent are 
highly sensitive to it. 

Treatment 

Symptomatic. 

moonseed (Menispermum canadense) [Other 
names: Canadian moonseed, Texas sarsaparilla, 
vine-maple, yellow sarsaparilla.] Sometimes mis- 
taken for wild grapes, moonseed is a woody twin- 
ing vine growing on stream banks and fences in 
eastern North America. Its Hawaiian relative, also 
called moonseed (Cocculus ferrandianus) , is used as 
a fish poison. A perennial, moonseed grows in the 
eastern part of the United States in moist woods, 
hedges, and streams. Its woody root is very long 
and yellow, and its stem is a climbing vine with 
round, smooth leaves and yellow flowers appear- 
ing in July, followed by one seeded fruit. 

Poisonous part 

Both leaves and fruit contain poisonous alkaloids. 

Symptoms 

Within several hours after ingestion, moonseed 
grapes and leaves cause bloody diarrhea, convul- 
sions, shock, and death. 

Treatment 

Gastric lavage. 

morning glory (Ipomoea) [Other names: flying 
saucer, heavenly blue, pearly gates.] This is the 
common name for plants of the Convolvulaceae 
family, which are popular for their hallucinogenic 
properties. These viney plants have large, heart- 
shaped leaves and flaring, brightly colored flowers; 
the hallucinogenic part of the plant is the black or 
brown seeds. The seeds' hallucinogenic properties 
have been known since ancient times, when Aztecs 
and North American Indians used them as part of 



their rehgious ceremonies and in healing and divi- 
nation. Not all species are toxic, however. 

In recent times, the seeds of the morning glory 
have been advertised for sale in alternative publi- 
cations as "hallucinogens" but also labeled "not for 
human consumption." 

Poisonous part 

The seeds of this plant are poisonous and contain 
an active principle similar to that of LSD, but only 
one-tenth as toxic. 

Symptoms 

Between 50 and 200 powdered seeds can produce 
symptoms similar to those caused by LSD, with feel- 
ings of depersonalization and visual hallucinations, 
in addition to psychoses and flashbacks later on. 

Treatment 

Supportive and symptomatic. Do not induce vom- 
iting; gastric lavage should be performed within 30 
minutes only in case of massive overdose. 



morphine [Other names: lanthopine, lauda- 
noisine, laudanum, meconidine, narcotine, 
protopine.] Considered to be supertoxic, this opi- 
ate is the principal alkaloid of opium and is the 
best-known narcotic painkiller. It is extracted from 
the unripe seed pods of the opium poppy. It has 
been used as a painkiller since 1886 and was often 
found in Chinese opium dens popular during the 
Victorian era. 

A white crystalline alkaloid, it is available in liq- 
uid or tablet form and can be ingested or injected. 
Liquid morphine is a bluish syrup given to cancer 
patients to treat pain, sometimes mixed with a blue 
hqueur to strengthen the effects. 

Morphine increases the effects of sedatives, pain- 
killers, sleep-inducing drugs, tranquilizers, antide- 
pressants, and other narcotic drugs. It works faster 
if mixed with alcohol or other solvents. It works by 
blocking the transmission of pain signals at specific 
sites in the brain and spinal cord, preventing the 
perception of pain. Short-term use is not hkely to 
cause dependence, but the euphoric effects of the 
drug have contributed to its long history as a street 



158 mothballs 



drug. Long-term abuse leads to a craving for the 
drug and a need to have ever-greater amounts. 
Sudden withdrawal of the drug can cause flu -like 
symptoms (sweating, shaking, and cramping). 

In addition, morphine cannot be used together 
with a wide range of drugs, including aminophylline, 
phenytoin, phenobarbital, and sodium bicarbonate. 

Symptoms 

Symptoms include sleepiness, physical ease, float- 
ing sensations, giddiness, unbalanced gait, dizzi- 
ness, nausea, breathing problems, unconsciousness, 
and coma. Depressant effects may last longer in 
those persons with liver or kidney problems. Death 
from morphine overdose occurs between six and 
12 hours after ingestion and is almost always due 
to respiratory failure. If the victim survives for two 
days, the prognosis is good. 

Treatment 

Naloxone is the antidote; recovery can be expected 
within one to four hours if administered soon after 
ingestion. 

See also heroin; naloxone; narcotics; opium. 



mothballs See camphor; naphthalene. 

mother-in-law plant (Caladium) This popular 
plant is cultivated both outdoors and as an indoor 
plant and can grow to about 16 inches. It is a 
deciduous plant with large, oval arrow-shaped 
leaves that can grow to be 14 inches long and come 
in a range of colors, including pink, red, white, 
and green. The plants can be cultivated all year 
in subtropical gardens and during the summer in 
temperate zones. 

Poisonous part 

All parts of the plant are toxic and contain raphides 
of calcium oxalate. 

Symptoms 

Ingestion causes pain, swelling, and irritation of 
the mouth, lips, throat, and the digestive tract, 
which leads to nausea, vomiting, and diarrhea. 
Ingestion of a large amount can result in swelling 



of the tongue and throat, which can obstruct the 
airway. 

Treatment 

Pain and swelling subside on their own, but cool 
liquids and demulcents (such as milk) held in the 
mouth may help the pain. Painkillers are sometimes 
given, but the oxalates in this plant are insoluble 
and therefore do not cause systemic poisoning. 

mountain laurel See laurel, mountain. 



MSG See monosodium glutamate. 



multiple chemical sensitivity (MCS) A physical 
illness clinical ecologists beheve is caused by min- 
ute levels of toxic chemicals in the air, water, and 
food. According to this theory, people with MCS 
suffer from fatigue, achy muscles, headaches, men- 
tal fogginess, and other vague symptoms because 
of sensitivity to tiny amounts of toxic chemicals in 
the environment. 

While many traditional physicians believe these 
ills are primarily psychosomatic, others believe 
there is evidence of a real chemical illness and that 
it may affect 15 percent of Americans. According to 
these clinical ecologists, the disease develops in one 
of two ways: through a slow buildup of chemicals 
over the years, or from one massive exposure such 
as an industrial chemical spill. 

People are more vulnerable if they have nutri- 
tional deficiencies, a family history of allergies, a 
chronic disease or an infection that has weakened 
the immune system. Still, experts recommend that 
health problems must be ruled out before concluding 
that the environment is to be blamed for illness. 

Even physicians who doubt the existence of 
MCS concede that it can't hurt to pay attention 
to chemicals and try to avoid overexposure. They 
recommend the following: 

• Store insecticides, paint thinner, and other toxic 
chemicals in an outside shed or garage; never 
keep them under the sink where the fumes can 
leak into the house. 



mushroom poisoning 159 



• Choose electric appliances, 100 percent cotton or 
wool carpets, and furniture made of glass, chrome, 
or solid wood instead of particleboard. Avoid "no 
chip" wood finishes that emit formaldehyde. 

• Keep gas appliances repaired; replace filters 
regularly. 

• Be cautious with chemicals used often: artists' 
oils, marking pens, and typewriter correction 
fluid can be highly toxic. 

• Air out the house often, especially when using 
appliances than burn gas, propane, wood, or 
kerosene. 

• Use your own nontoxic products: use fresh herbs 
and flowers as air fresheners; dust with pure min- 
eral oil sweetened with drops of lemon; soften 
fabrics by adding baking soda to rinse water. 

• Air dry-cleaned clothes, bedspreads, and drapes 
outside before bringing them into the house. If 
dry-cleaned goods have a chemical odor, refuse 
to accept them until they are properly dried; 
change cleaners if the problem persists. 

• Read and follow labels; wear gloves and open 
windows when using mildew removers, rug 
shampoos, or other household chemicals. 

• Wash permanent-press clothes and sheets before 
using, or buy all-natural fibers (wool, cotton, 
and silk). 

• Avoid pesticides. 

• Don't smoke. (Cigarette smoke contains 4,700 
chemicals, according to the Environmental Pro- 
tection Agency. ) 

muscarine This alkaloid was isolated in 1869 as 
a minor toxic constituent in the mushroom Ama- 
nita muscaria (in fresh fungi, it is found in only a 
concentration of 0.0003 percent). It is found in 
much larger amounts in many species of Inocybe 
and some species of Clitocybe mushrooms. Eating 
mushrooms that contain muscarine is only rarely 
fatal; even without treatment, most symptoms fade 
within a few hours. 

Symptoms 

Muscarine, like pilocarpine, excites receptors of 
the parasympathetic and sympathetic nervous sys- 



tems. Within 1 5 to 24 hours after ingestion, mus- 
carine poisoning produces profuse sweating and 
salivation, visual disturbances, nausea, vomiting, 
abdominal pain, diarrhea, headache, and broncho- 
spasm. Very high doses cause incontinence, slow 
heartbeat, low blood pressure, and shock. 

Treatment 

Symptoms will disappear even without treatment 
in most cases. However, vomiting and gastric 
lavage may help together with the administration 
of atropine to suppress toxin symptoms. 

See also Amanita mushrooms; fly agaric; ino- 
cybe mushrooms; mushroom poisoning; mush- 
room TOXINS. 

muscimol This water-soluble toxin was first iso- 
lated in the early 1960s from the toxic mushrooms 
Amanita muscaria (or fly agaric) and Amanita pan- 
therina (panther mushroom). Both muscimol and 
its metabolic precursor ibotenic acid are believed to 
be the primary cause for the toxicity of these two 
mushrooms and a few related species. 

Symptoms 

Within 20 to 90 minutes after ingestion, muscimol 
begins to affect the central nervous system, causing 
drowsiness, stupor, elation, hyperactivity, dehrium, 
confusion, hallucinations, rapid heartbeat, gastro- 
enteritis, and urinary retention. 

Treatment 

Induce vomiting and perform gastric lavage; admin- 
istration of physostigmine and diazepam (Vahum) 
may help control symptoms and convulsions. 
Stimulants are not advised. 

See also Amanita mushrooms; fly agaric; 
mushroom poisoning; mushroom toxins; panther 
mushroom. 



mushroom poisoning There is a reason for 
the saying "There are old mushroom hunters, 
and bold mushroom hunters, but no old bold 
mushroom hunters." In recent years, cases of 
mushroom poisoning have been on the increase, 
attributable to the rise of interest in "natural" 



160 mushroom poisoning 



foods and to better reporting of cases. At tfie same 
time, scientists liave been learning more and more 
about the toxic properties of mushrooms, or "fun- 
gus fruit." 

Out of the more than 5,000 varieties of mush- 
rooms found in the United States, about 100 are 
toxic — but most of these cause only mild stomach 
problems. A few, however, can cause fatal reac- 
tions. Most of the toxic symptoms are caused by 
the gastrointestinal irritants that lead to the vomit- 
ing and diarrhea common in mushroom poisoning. 
In most cases, onset of stomach distress is rapid, 
but if the onset is delayed past six to 12 hours, the 
more serious amatoxin or monomethylhydrazine 
poisoning may be suspected. The stalk and cap of 
the mushroom that pops up after a spring rain are 
really the fruit of a vast underground network of 
microscopic filaments; therefore, picking a mush- 
room no more harms the plant than plucking an 
apple from a tree. 

But despite the fact that scientists for the past 
hundred years have been trying to isolate the 
toxic principles in mushrooms, the exact chemistry 
behind the deadly poisons in these fungi is still 
unknown. While most of the species of mushroom 
are not poisonous, the few toxic ones that do exist 
are deadly and have been known since ancient 
times. 

Since the first report of mushroom poisoning in 
1871, much of the information about poisonous 
mushrooms is inaccurate — including the persistent 
belief that there are some ironclad "rules" that can 
be used to tell the difference between edible and 
toxic varieties. In fact, there is no rule that apphes 
to all species of mushrooms. 

For example, it's not true that a silver spoon or 
coin put in a pan with cooking mushrooms will 
turn black if the mushrooms are poisonous. All 
mushrooms will discolor silver in boiling water, if 
they are rotten, but no mushroom (toxic or edible) 
ever does as long as it is fresh. Toxic mushrooms 
won't get darker if soaked in water, nor will they 
get milky if soaked in vinegar. 

A mycologist (mushroom expert) is the only 
one who can reliably detect poisonous mushrooms, 
and even mycologists make mistakes because the 
toxicity of mushrooms is complicated. Some are 
always deadly; others are poisonous at some times 



MUSHROOMS GROUPED ACCORDING 
TO PRIMARY TOXIN 

Amatoxins and Phallotoxins (cyclopeptides) 

Amanita phalloides A. tenuifolia 

A. verna Galerina autumnalis 



A. virosa 
A. bisporigera 
A. ocreata 
A. suballiacea 



C. marginata 
G. venenata 
Lepiota helveola 
Conocybe filaris 
Muscimol and Ibotenic Acid 
Amanita muscaria A. colieri 
A. pantherina A. cothurnata 

A. gemmata A. Strobiliformis 
Monomethylhydrazine (gyromitrins) 
Gyromitra esculenta G. brunnea 

G. gigas G. fastigiata 

G. ambigua Paxina 

G. infula Sarcosphaera coronaria 

C. caroliniana 

Muscarine 

Boletus calopus I. geophylla 

B. luridus I. lilacina 

B. pulcherrimus I. patouillardii 

B. satanas I. purica 
CUtocybe cerrusata I. rimosus 

C. dealbata Amanita muscaria 
C. illudens A. pantherina 

C. riuulosa 

Inocybe fastigiata 

Coprine (and Cyclopropanone) 

Coprinus atramentarius 

CUtocybe clavipes 

Indoles (psilocybin and psilocin) 

Psilocybe cubensis P. silvatica P. semilanceata 

P. caerulescens Conocybe cyanopus Stropharis coronilla 

P. cyanescens Gymnopilus aeruginosa 

P. baeocystis G. spectabilis 

P. fimentaria G. validipes 

P. mexicana Panaeolus foenisecii 

P. pelluculosa P. subbalteatus 



but not others, depending on the stage of growth. 
And other poisonous mushrooms have never been 
regarded as toxic simply because no one has ever 
eaten them yet. 



mushroom poisoning 161 



The most common poisonous mushrooms in 
the United States are those in the genus Amanita 
(including the world's deadhest mushroom, A. 
phalloides); up to 90 percent of those who eat this 
mushroom will die if untreated. 

Unlike most incidents of plant poisonings, which 
occur primarily in curious children, poisoning from 
mushrooms is generally found among adults who 
ingest them as a source of food or for their halluci- 
nogenic effects. While it may be easier to obtain a 
history of the ingestion, it is usually almost impos- 
sible to identify the kind of mushroom eaten. It is 
possible, however, to identify the type of mushroom 
by evaluating the kinds of symptoms, since mush- 
rooms produce only a small number of distinct toxic 
syndromes. 

Identification 

It's possible to identify the kind of mushroom 
ingested based on the following questions: 

1 . When was the mushroom eaten, and how long 
afterward did the symptoms appear? (When 
symptoms develop within two hours of inges- 
tion, they are not often severe. Poisonings with 
a latency period of more than six hours may be 
severe or life threatening.) 

2. What symptoms appeared first? If symptoms 
appeared quickly, are they primarily 

• nausea and stomach pain with vomiting/ 
diarrhea? 

• sweating? 



• intoxication or hallucinations but no 
drowsiness? 

• delirium and sleepiness or coma? 

If symptoms were delayed, did they produce 

• a feeling of fullness and severe headache six 
hours later? 

• vomiting and watery diarrhea about 1 2 hours 
after eating? 

• extreme thirst and copious urination three 
days after eating? 

If someone who did not eat mushrooms shows 
similar symptoms, it's possible the problem is bac- 
terial food poisoning and not mushroom poisoning 
at all. 

Symptoms 

In general, symptoms that appear within two 
hours of eating poisonous mushrooms are rarely 
severe and require little intervention; symptoms 
that do not appear until six or more hours later 
are usually much more severe and can be life 
threatening. If more than one type of mushroom 
was eaten, several types of toxicity may occur. 
However, symptoms that appear after eating 
mushrooms may not be the result of systemic 
poisoning from a toxic mushroom. Some people 
are allergic to mushrooms, and others have a 
genetic deficiency of enzymes needed to metabo- 
lize the unusual sugars found in mushrooms; this 



MUSHROOM TOXICITY 



Mushroom 


Toxin 


Symptoms 


Amanita muscaria, A. pantherina and others 


Ibotenic acid, muscimol 


Muscle jerks, hallucinations 


Amanita phalloides, A. ocreata, A. verna, 
A. virosa, Lepiota and Galerina species 


Amatoxins 


Vomiting, diarrhea, cramps, liver 
failure 


Clitocybe dealbata, Inocybe species, 
C. cerrusata, Omphalotus olearius 


Muscarine 


Salivation, sweats, vomiting, 
diarrhea, miosis 


Coprinus, Clitocybe clavipes 


Coprine 


Reaction with alcohol 


Gyromitra (l-lelvella) esculenta and others 


Monomethylhydrazine 


Vomiting, diarrhea, weakness, sei- 
zures, hepatitis, hemolysis 


Psilocybe cubensis and others 


Psilocybin 


Hallucinations 



162 mushroom toxins 



deficiency causes gas and diarrhea. If alcohoiic 
beverages were drunk within 72 hours of eat- 
ing mushrooms, extreme nausea, vomiting, and 
headache could occur as a result of the interfer- 
ence of edible mushrooms with the metabolism 
of alcohol. 

Treatment 

If someone becomes sickened and mushroom 
poisoning is suspected, first find out how many 
types of mushrooms were eaten, when they were 
eaten, the symptoms and if anyone else ate them. 
When determining symptoms, find out which 
ones appeared first. Gastrointestinal symptoms 
that appear more than six hours after ingestion 
are usually caused by a group of mushrooms 
including the deadly amanitas, or mushrooms 
containing monomethylhydrazine (including 
Gyromitra mushrooms, or false morels). If the 
victim has not already vomited, administer syrup 
of ipecac followed by activated charcoal and 
a cathartic. If possible, send vomited material, 
together with any remaining mushrooms, to a 
mycologist for identification. If ingested mush- 
room is of the Amanita species (except for A. 
muscaria or A. pantherina), the victim should be 
admitted to the hospital to monitor kidney and 
liver function. 



See also amatoxins; coprine; Gyromitra; mono- 
methylhydrazine; muscarine; muscimol; mush- 
room TOXINS. 



mushroom toxins Any illness due to the inges- 
tion of a toxic mushroom (or toadstool) is known 
as mycetismus. Many species of wild mushrooms 
in many genera are poisonous; several of the toxins 
have been isolated and identified. It is important 
to remember that mushroom toxins differ among 
themselves and in the type of intoxication and 
symptoms they produce. 

Poisoning by a mushroom toxin might range 
from mild symptoms of stomach upset to fatal dis- 
turbances of the body's major systems, including 
brain, heart, liver, and kidneys. 

Of the approximately 5,000 different types of 
mushrooms in the United States, about 100 are 
poisonous and less than a dozen can be deadly. 
Amanita mushrooms account for 90 percent of 
deaths related to mushrooms. 

See also Amanita mushrooms; amatoxin; 
coprine; fly agaric; galerina mushrooms; 
Gyromitra; hallucinogenic mushrooms; inky cap; 
iNOCYBE mushroom; lepiota mushrooms; mono- 
methylhydrazine; muscarine; muscimol; mush- 
room poisoning; turbantop. 



N 



naloxone This opioid drug bloclts the action of nar- 
cotic drugs and reverses breathing difficulty caused by 
a narcotics overdose. It is also given to newborn babies 
who are affected by narcotics during childbirth, and 
to patients who have received high doses of a narcotic 
drug during surgery. In addition, some reports sug- 
gest that naloxone may at least partially reverse the 
central nervous system and respiratory depression 
following clonidine and ethanol overdoses. 

See also heroin; morphine; narcotics; opium. 

nanophyetiasis This type of infestation is caused 
by eating seafood tainted with worms (Nanophyetus 
salmincola or N. schikhobalowi) that are transmitted 
as a larvae that embeds itself in the flesh of fresh- 
water fish. There have been no reports of massive 
outbreaks; the only scientific report has been an 
account of 20 people in Oregon who came down 
with the disease. However, the condition is endemic 
in Russia, where the infection rate is reported to be 
more than 90 percent and growing. North Ameri- 
can cases were aU associated with raw, smoked, 
and underprocessed salmon and steelhead. 

Symptoms 

Diarrhea, usually accompanied by stomach discom- 
fort and nausea; a few people reported weight loss 
and fatigue. 

Diagnosis 

The disease is diagnosed by finding the eggs in feces. 
However, it's hard to tell the difference between 
these eggs and those of another parasite {Diphyl- 
lohothrium latum). 

Treatment 

Treatment with niclosamide or bithionol appears to 
cure the infection. 



naphthalene More commonly known as moth- 
balls or mothball flakes and contained in toilet bowl 
cleaners, naphthalene is a white crystalline solid 
and a constituent of coal tar, which can be poison- 
ous when eaten. In the past, naphthalene has also 
been used as an antiseptic; however, naphthalene 
is no longer commonly used because it has been 
replaced by the far less toxic paradichlorobenzene. 

Too often, parents do not realize how toxic moth- 
balls are and leave them out where toddlers can 
eat them. In addition, naphthalene does not easily 
dissolve in water and so many remain in clothes or 
blankets even after washing. It's even more danger- 
ous to store baby clothes in mothballs, since naph- 
thalene is very soluble in oil; the baby oil rubbed on 
an infant's skin acts as a solvent for the toxic sub- 
stances in the clothes, which can then be absorbed 
in the baby's skin. Naphthalene products should 
never be used with children's clothes and diapers. 

Symptoms 

Symptoms appear quickly, within five to 20 min- 
utes depending on whether naphthalene was 
inhaled or eaten. First symptoms are nausea, vom- 
iting, headache, diarrhea, fever, jaundice, and pain 
while urinating. More serious poisoning causes 
excitement, coma, and convulsions. Naphthalene 
causes kidney damage and destroys red blood ceUs, 
clumping them together and forcing the hemoglo- 
bins out. People with a hereditary deficiency of 
glucose-6-phosphate dehydrogenase (most often 
people of Mediterranean descent) are more sus- 
ceptible to naphthalene poisoning. This same defi- 
ciency makes them sensitive to aspirin. 

Treatment 

There is no specific antidote. If ingested, perform 
immediate gastric lavage followed by a saline 



163 



164 naproxen 



cathartic; alcohol, milk, oil, or fats should be 
avoided. Drink plenty of fluids to encourage the 
production of urine, and administer sodium bicar- 
bonate orally and fluids with furosemide to stop 
kidney damage. With severe cases of poisoning 
with central nervous system problems, blood trans- 
fusions are given. 

See also paradichlorobenzene. 



naproxen (Naprosyn) See nonsteroidal anti- 

INELAMMATORY DRUGS. 



narcissus (Narcissus) This extremely toxic plant 
genus includes about 26 varieties of common 
flowering plants with hundreds of cultivars; they 
include popular plants such as the jonquil {N. 
jonquilla) and the daffodil (N. pseudonarcissus) — all 
of which are poisonous. While native to central 
Europe and North Africa, they are found through- 
out the United States. 

Poisonous part 

All parts of these plants — especially the bulbs — are 
poisonous and contain lycorine and other alkaloids. 

Symptoms 

Even small amounts of the bulbs can cause poison- 
ing in adults within several hours to a few days, 
including symptoms of nausea, severe vomiting, 
diarrhea, and colic. If eaten in large quantities, 
narcissus can cause convulsions, collapse, paralysis, 
and death. Mortality is about 30 percent. 

Treatment 
Gastric lavage and fluid replacement. 

narcotics A group of depressants including 
codeine, opium, morphine, paregoric, and heroin, 
which are used medicinally to relieve pain, cough- 
ing, and vomiting. They require a doctor's prescrip- 
tion, since continued use can lead to dependence 
or addiction. 

Depressants in addition to the above include 
fentanyl or Subhmaze; the eye drop DPP or diiso- 
propylphosphate; Numorphan (oxymorphone); 



the painkiller Dilaudid (hydromorphone); the 
cough suppressant Hycodan or Dicodid; Lorfan 
(levallorphan); Levo-Dromoran (levorphanol); the 
painkiller Darvon (propoxyphene); the painkiller 
Talwin (pentazocine); the muscle relaxant Flex- 
eril (cyclobenzaprine); Demerol (meperidine); and 
Dolantin (pethidine). 

Symptoms 

Soon after ingestion, the victim will become men- 
tally stimulated and then quickly drowsy. As the 
body continues to absorb the narcotic, the victim 
will experience headache, slow, shallow breathing, 
and finally unconsciousness and coma. 

Treatment 

Medical help should be sought immediately. Stimu- 
lants, such as strong tea and coffee, will help to keep 
the victim awake. If the victim is discovered soon 
after ingestion and is conscious, induce vomiting. 

See also codeine; heroin; hydromorphone; 
morphine; opium; oxymorphone. 

Nembutal See barbiturates. 



neostigmine See parasympathomimetic drugs. 

neuromuscular blocking agents A group of drugs 
that paralyze skeletal muscles, used to counteract 
excessive muscular activity, rigidity, or seizures 
following overdoses involving stimulants (amphet- 
amines, cocaine, phencyclidine) or strychnine. The 
drugs include succinylcholine, pancuronium, and 
vecuronium. They are also used to help paralyze 
muscles prior to placement of an ototracheal tube. 
See also amphetamines; cocaine; strychnine. 

neurotoxic shellfish poisoning This type of toxic 
poisoning is associated with shellfish harvested 
along the coasts of Florida, North Carolina, and 
the Gulf of Mexico. The toxin attacks the nervous 
system and triggers both stomach and neurologi- 
cal problems. Recovery is complete with very few 
after-effects; no fatalities have been reported. 



nicotine 165 



Symptoms 

Symptoms occur within a few minutes to a few 
hours after eating contaminated shellfish and 
include tingling and numb lips, tongue and throat, 
muscular aches, dizziness, reversal of sensations, 
diarrhea, and vomiting. Symptoms last between a 
few hours and a few days. 

Prevention 

Monitoring programs can prevent human intoxica- 
tion. Consumers should eat shellfish from report- 
able sources and approved beds only. 

neutral izers Rarely used in modern hospitals, 
neutralizing agents at one time were sometimes 
employed instead of activated charcoal in cer- 
tain poisoning cases: mercury and iron poisoning, 
iodine ingestion, and strychnine, nicotine, and 
quinine poisoning (see below). 

Mercury 

Sodium formaldehyde sulfoxylate neutralizes 
mercuric chloride and other mercury salts to 
metallic mercury, which cannot be absorbed by 
the body. 

Iron 

Gastric lavage with sodium bicarbonate converts 
the ferrous ion to ferrous carbonate, which is not 
well absorbed by the body. 

Strychnine, nicotine, and quinine 

Administer potassium permanganate. 

Iodine 

Gastric lavage with a solution of starch and water, 
which is continued until the stomach contents are 
no longer blue. 

See also charcoal, activated; iodine; iron sup- 
plements; mercury; nicotine; potassium perman- 
ganate; quinine; sodium bicarbonate; strychnine. 

nicotinamide One of the B vitamins used to pre- 
vent toxic effects in the brain and endocrine system 
following the ingestion of the rat poison Vacor. 
See also Vacor. 



nicotine A plant alkaloid found in several spe- 
cies of tobacco and an extremely fast-acting poison 
that, when eaten, can cause blood vessels to col- 
lapse and the muscles of respiration to fail in much 
the same way as does curare. While there is no 
medicinal use for nicotine, some of its derivatives 
are used as botanic insecticides; in fact, nicotine is 
the oldest insecticide known. 

In those who ingest nicotine by smoking ciga- 
rettes or chewing the leaves, repeated small doses 
soon build up tolerance to the toxins. The primary 
danger of poisoning lies in the manufacture and 
use of insecticides containing nicotine. 

Toxic doses vary and range from four milhgrams 
to two grams; generally 40 milligrams is considered 
fatal. Nicotine content in regular cigarettes aver- 
ages about 15 to 20 milligrams per cigarette; cigars 
range from 15 to 40 milligrams. Eating tobacco is 
not generally a serious toxic risk, since the stomach 
does not absorb nicotine well from cigarettes. 

Children may become poisoned with nicotine 
if they ingest tobacco or drink saliva spit out by 
a tobacco chewer (often collected in a spittoon 
or can). Adults may attempt suicide by ingesting 
nicotine -containing pesticides, or may be poisoned 
after coming in contact with tobacco while harvest- 
ing the plants. 

Nicotine chewing gum (Nicorette) has been 
marketed as an aid for people to stop smoking, but 
its slow absorption makes nicotine intoxication 
from this product unlikely. 

Symptoms 

Nicotine's effects are extremely complex and vary 
from person to person, depending on the length 
of time following exposure, the amount of dosage 
and chronic use. Cigarette tobacco and moist snuff 
each contain about 1.5 percent nicotine; chew- 
ing tobacco contains 2.5 to 8 percent nicotine; 
nicotine gum contains two milligrams per piece in 
the United States (although bioavailability is only 
about 20 to 40 percent of that amount). 

Rapid absorption of between two and five mil- 
ligrams can cause nausea and vomiting, especially 
in a person unused to nicotine. Absorption of 40 to 
60 milligrams in an adult may be lethal, although 
most smokers get this dose spread throughout the 
day. In a child, ingestion of one cigarette or three 



166 nicotine gum 



butts may be toxic, although serious poisoning 
from cigarette ingestion is rare. 

Immediately after ingestion, nicotine causes a 
burning sensation in the mouth, throat, esopha- 
gus, and stomach. Once in the bloodstream, 
whether after inhalation from tobacco smoke or 
through the mouth from chewing tobacco (or, 
more recently, in nicotine gum or the nicotine 
skin patch), the substance acts on the central ner- 
vous system until it is eventually broken down 
by the liver and excreted. It first stimulates, and 
then depresses, both the brain and spinal cord. It 
primarily affects the autonomic nervous system, 
which controls involuntary body activities (such 
as heart rate). While effects vary from person to 
person, it can slow the heart rate and cause nau- 
sea and vomiting. 

In habitual users, however, nicotine increases 
the heart rate, narrows the blood vessels (thereby 
raising blood pressure), and stimulates the central 
nervous system, reducing tiredness and improving 
concentration. It is uncertain whether the nicotine 
contained in tobacco products is responsible for 
coronary heart disease, peripheral vascular disease, 
and other heart problems. 

Extremely large amounts of nicotine can affect 
breathing in ways similar to that of curare, paralyz- 
ing the breathing muscles and causing vomiting, 
seizures, and death from respiratory arrest only 
minutes after ingestion. 

Treatment 

In severe poisonings, artificial respiration and 
oxygen must be administered, since death occurs 
from respiratory paralysis. Nicotine is completely 
eliminated from the body within 16 hours, so vic- 
tims who can be kept alive for that period may live. 
Mecamylamine (Inversine) is a specific antagonist 
of nicotine but is available only in tablets, which 
are not suitable for a victim who is vomiting, has 
low blood pressure or is having convulsions. Signs 
of parasympathetic stimulation (that is, slow heart- 
beat, salivation, wheezing, etc.) may respond to 
atropine. 

For ingestion: gastric lavage followed by the 
administration of activated charcoal to absorb 
excess nicotine; pentobarbital, diazepam, or inha- 
lation anesthesia to control convulsions. For skin 



contamination: scrub skin with plenty of soap and 
water and remove contaminated clothing. 

See also alkaloids; botanic insecticides; nico- 
tine gum; nicotine patch; tobacco. 

nicotine gum (nicotine polacrilex) Popularly 
known by its trade name Nicorette, this is a 
nicotine resin that is used to help people stop 
smoking. It gradually releases nicotine when 
chewed. However, chewing too much of the gum 
will release too much nicotine and cause nausea. 
For this reason, heart patients, pregnant women, 
and those with peptic ulcers should not chew the 
gum. 

The gum was designed to be "parked" between 
cheek and gum, in order to maximize the nicotine's 
absorption. As the smoker begins to feel comfort- 
able with the smoke-free behaviors, the amount 
of nicotine is decreased over a six-month period. 
Lower- strength versions are available without a 
prescription. A doctor can decide which strength is 
needed. Drinks will wash the nicotine to the stom- 
ach, so it needs to be absorbed by the mouth. Ten 
to 15 pieces a day is a normal dose. 

Symptoms 

The same as nicotine overdose. 

Treatment 

For severe overdose, see Treatment section under 
nicotine. 

See also nicotine; tobacco. 

nicotine patch Another innovation in the stop- 
smoking arsenal, the nicotine patch became avail- 
able in the United States in 1994. In this form, 
nicotine is gradually absorbed through the skin as a 
means to help a smoker stop using cigarettes. 

Since the introduction of nicotine gum and the 
transdermal patch, estimates based on FDA and 
pharmaceutical industry data indicate that more 
than I milhon individuals have been successfully 
treated for nicotine addiction. However, recent 
research reports indicate that several patients wear- 
ing a patch have died from heart attacks because 
they have continued to smoke. 



nightshade, bittersweet 167 



In 1996, a nicotine nasal spray, and in 1998, a 
nicotine inhaler, became available by prescription. 
Various comparisons of the effectiveness of the many 
nicotine-replacement products show a wide range of 
results. One study found that 1 1 percent of people 
who used a nicotine patch quit smoking, compared 
to 4.2 percent for those who used a placebo patch. 
A nonnicotinic medication called bupropion led to 
an abstinence rate of 30.3 percent after one year 
compared to a 16.4 percent rate for those using only 
the patch. A 2008 study found that after six months, 
42 percent of those using bupropion alone stopped 
smoking, compared to a 35 percent rate for those 
who used both a patch and the drug. Other studies 
show the nasal spray and nicotine inhalers to be 
more effective than the patch. 

Symptoms 

Nicotine acts on the central nervous system until 
it is eventually broken down by the liver and 
excreted. It first stimulates, and then depresses, 
both the brain and spinal cord. It primarily affects 
the autonomic nervous system, which controls 
involuntary body activities (such as heart rate). In 
habitual users nicotine increases the heart rate and 
narrows the blood vessels (thereby raising blood 
pressure); it can also cause a heart attack. 

Treatment 

The best treatment is preventive: Never smoke ciga- 
rettes while wearing a nicotine patch. In severe cases, 
artificial respiration and oxygen may need to be 
administered. Nicotine is completely eliminated 
from the body within 1 6 hours, so victims who can 
be kept alive for that period may live. Mecamyla- 
mine (Inversine) is a specific antagonist of nicotine 
but is available only in tablets, which are not suit- 
able for a victim who is vomiting, has low blood 
pressure or is having convulsions. Signs of parasym- 
pathetic stimulation (that is, slow heartbeat, saliva- 
tion, wheezing, etc.) may respond to atropine. 
See also nicotine; nicotine gum; tobacco. 

nifedipine This substance dilates the arteries and 
is used to combat severe high blood pressure fol- 
lowing overdose of artery-constricting drugs such 
as phenylpropanolamine, cocaine, amphetamines. 



phencyclidine, (PCP) or other stimulants. It is also 
helpful to counteract peripheral or coronary artery 
spasms following poisoning by ergot or cocaine. 

See also amphetamines; cocaine; ergot; 
phencyclidine. 



nightshade, bittersweet A member of the wide- 
ranging nightshade family (but a less deadly relative 
than deadly nightshade), bittersweet nightshade 
can also have poisonous effects. 

Poisonous part 

The entire plant contains the toxin atropine and 
other belladonna alkaloids, including scopolamine, 
hyoscyamine, hyoscine, and belladonna — but these 
are concentrated in the roots, leaves, and berries. 
These alkaloids paralyze the parasympathetic ner- 
vous system (which controls the involuntary activ- 
ities of the organs, glands, blood vessels, and other 
body tissues). Atropine can directly stimulate the 
central nervous system and is eliminated almost 
entirely by the kidneys. Taken internally, as little as 
0.1 gram of atropine (one of the alkaloids extracted 
from nightshade) can cause poisoning. 

Symptoms 

Symptoms appear between 15 minutes and a 
few hours after ingestion and include a scratchy 
or burning sensation in the throat with a loss of 
voice, rapid pulse, fever, nausea, vomiting, blurred 
vision, pupil dilation, inability to urinate, difficulty 
in swallowing, mental confusion, aggressive behav- 
ior, reduced secretion of saliva, convulsions, coma, 
and death. The poison acts by paralyzing the nerve 
endings of the involuntary muscles. Mild poisoning 
acts as a euphoric, imparting a feeling of timeless- 
ness or giddiness to its victims. Severe poisoning 
causes blindness, rage, and paralysis of the central 
nervous system. Coma is followed by death from 
respiratory failure. 

Treatment 

Gastric lavage with 4 percent tannic acid solution 
and vomiting. Pilocarpine or physostigmine may 
be given for dry mouth and visual disturbances. 
There is no known antidote. There is risk of heart, 
kidney, and urinary tract damage if symptoms are 



168 nightshade, deadly 



prolonged or severe. If treatment is initiated, prog- 
nosis is good. 

See also atropine; nightshade, deadly. 



nightshade, deadly (Atropa belladonna L.) [Other 
names: anuncena de Mejico, banewort, Barba- 
dos lily, belladonna lily, cape belladonna, dwale, 
English nightshade, lirio, naked lady lily, sleeping 
nightshade.] Also known as belladonna, deadly 
nightshade is a powerful drug plant (source of the 
drug atropine) with a history rich in magic, witch- 
craft, and murder. It is a member of the Solanaceae 
family and is one of a group of nightshades. 

However, the "true" nightshades contain the 
poison solanine, and they are closely related — the 
Jerusalem cherry, the woody nightshade or Euro- 
pean bittersweet, and the American, or black, 
nightshade. Deadly nightshade (the belladonna 
plant) belongs to another branch of the Solana- 
ceae, and its chief poison is atropine. 

Atropine and solanine have different effects on 
the body, so that reporting a poisoning with "night- 
shade" is not specific enough to determine correct 
treatment. 

Native to Eurasia and North Africa, this five- 
foot, shrublike perennial herb is found in mead- 
ows, near old buildings, and in shady, marshy 
places in North America and is cultivated com- 
mercially in Europe for medicinal purposes. While 
its fresh leaves have an unpleasant smell when 
crushed, the dried leaves are odorless; both have a 
bitter taste. Its alternate ovate leaves grow on mul- 
tibranched stems, with glossy black, round berries 
and bellshaped flowers that have an intensely 
sweet smell from July to September. A horizon- 
tal, underground, thickened plant stem produces 
shoots above and roots below and bears buds, 
nodes, and scalelike leaves. 

The name "belladonna" comes from the Italian, 
meaning "beautiful woman," a reference to its use 
during the Renaissance, when women used an 
extract to make their complexions luminous and to 
dilate their pupils for a wide-eyed, beautiful look. 
Rouge was also made from the berries. Its generic 
name Atropa comes from the Greeks, whose myth 
holds that when the thread of life was played out 
by the three Fates, Atropos cut it. 



According to astrologists, deadly nightshade is 
ruled by Hecate and is popular in witchcraft as 
a shape changer, a flying ointment, and a major 
hallucinogen. (Of 16 recipes for flying ointments, 
eight call for deadly nightshade.) It is also said 
that deadly nightshade can change into a beauti- 
ful enchantress on Walpurgis Night, the witches' 
sabbath. 

There is also a place for nightshade in literature; 
it is believed Shakespeare intended it as the poison 
that Juhet takes in Romeo and Juliet so she wifl seem 
dead but is really just sleeping. 

Poisonous part 

A single berry can be fatal, and the entire plant 
contains the toxin atropine and other befladonna 
alkaloids, including scopolamine, hyoscyamine, 
hyoscine, and belladonna — but these are concen- 
trated in the roots, leaves, and berries. These alka- 
loids paralyze the parasympathetic nervous system 
(which controls the involuntary activities of the 
organs, glands, blood vessels, and other body tis- 
sues). Atropine can directly stimulate the central 
nervous system and is eliminated almost entirely 
by the kidneys. 

Taken internally, as little as O.I gram of atropine 
(one of the alkaloids extracted from nightshade) 
can cause poisoning. The root is the most poison- 
ous part, but the entire plant is deadly. A careful 
dose of deadly nightshade is antispasmodic, is a 
sedative and a diuretic and induces sweating; it 
also inhibits mucus and glandular secretions. At 
certain doses, the drug relieves pain and stimu- 
lates the central nervous system; it is classified as 
a narcotic. Its derivative atropine is considered an 
important drug today as an antidote for some types 
of nerve gas, and also as an antidote for depres- 
sant poisons such as muscarine, opium, and chlo- 
ral hydrate. Atropine is also an antispasmodic to 
treat gastritis, pancreatitis, and chronic urethritis. 
Nightshade's leaves provide isolated compounds 
including hyoscyamine and scopolamine, and it 
was once used in ophthalmology for pupil dilation, 
although it has generally been replaced today by 
other chemicals. 

The plant is often eaten by rabbits, which can 
then pass the poison on to anyone who eats the 
affected meat. 



nitrogen oxides 169 



Symptoms 

Symptoms appear between 15 minutes and a 
few hours after ingestion and include a scratchy 
or burning sensation in the throat with a loss of 
voice, rapid pulse, fever, nausea, vomiting, blurred 
vision, pupil dilation, inability to urinate, difficulty 
in swallowing, mental confusion, aggressive behav- 
ior, reduced secretion of saliva, convulsions, coma, 
and death. The poison acts by paralyzing the nerve 
endings of the involuntary muscles. Mild poisoning 
acts as a euphoric, imparting a feeling of timeless- 
ness or giddiness to its victims. Severe poisoning 
causes blindness, rage, and paralysis of the central 
nervous system. Coma is followed by death from 
respiratory failure. 

Treatment 

Gastric lavage with 4 percent tannic acid solution 
and vomiting. Pilocarpine or physostigmine may be 
given for dry mouth and visual disturbances. There 
is no known antidote for belladonna poisoning, and 
because the poison breaks down very slowly in the 
body, it is often impossible to save the victim. There 
is risk of heart, kidney, and urinary tract damage if 
symptoms are prolonged or severe, and poisoning 
can be quickly fatal if treatment is not initiated. If 
treatment is initiated, prognosis is good. 

See also atropine; nightshade, bittersweet; 

SOLANINE. 



nightshade, yellow (Urechites lutea) This woody 
vine is found in Florida, the Bahamas, and the 
Greater and Lesser Antilles south to St. Vincent. It 
has a milky sap and long, narrow leaves with yellow 
flower clusters. The fruit is contained in woody pods 
that can grow to 8 inches, containing winged seeds. 

Poisonous part 

The leaves of the yellow nightshade are poisonous, 
containing urechitoxin, a cardiac glycoside. 

Symptoms 

Symptoms appear some time after ingestion, 
depending on the amount of material eaten. They 
include pain in the mouth; nausea and vomiting; 
abdominal pain; cramps and diarrhea; and heart 
problems (conduction defects and slow heartbeat). 



Treatment 

Gastric lavage followed by activated charcoal and 
saline cathartics. For heart problems, atropine, and 
phenytoin. 

See also cardiac glycosides; nightshade, bit- 
tersweet; NIGHTSHADE, DEADLY. 

nitrogen oxides Nitric oxide and nitrogen diox- 
ide are dangerous chemical gases released during 
a variety of chemical and industrial processes, 
including electric arc welding, electroplating, 
and engraving. The oxides are found in engine 
exhaust, and they are produced when stored grain 
with a high nitrite content ferments in storage 
bins. Nitrogen dioxide is a colorless gas, arising 
from unvented gas stoves, that causes respiratory 
problems in children. 

Slow accumulation and hydration to nitric 
acid in the alveoli cause delayed onset of chemi- 
cal pneumonitis. Because nitrogen oxides do not 
dissolve well in water, there is very little upper 
respiratory irritation at low levels of exposure, 
and prolonged contact may occur with only a 
mild cough or nausea. However, with more con- 
centrated exposures, upper respiratory symptoms 
such as burning eyes, sore throat, and painful 
cough may be noted. 

Symptoms 

After exposure, there may be a delay of up to 24 
hours before chemical pneumonia may occur, 
with cough and pulmonary edema; following 
recovery there may be permanent restrictive and 
obstructive lung disease because of broncholar 
damage. 

Treatment 

Administration of corticosteroids is the treatment 
of choice by many toxicologists, but there is no 
convincing evidence that this will improve the 
chances of avoiding chemical pneumonia or lung 
damage. Remove the victim from exposure and 
give oxygen; observe closely for signs of upper 
airway obstruction for at least 24 hours after 
exposure. Remove contaminated clothing and 
flush exposed skin with water; irrigate exposed 
eyes with saline. 



170 nitroglycerin 



nitroglycerin (glyceryl trinitrate) A drug used to 
lower blood pressure and dilate coronary vessels; 
when taken with alcohol, it can cause a sharp drop in 
blood pressure. It is available in spray or tablet form 
and can be ingested, injected, inhaled, or absorbed. 
Nitroglycerin is also given to treat coronary spasm in 
adults suffering from ergot poisoning. 

Symptoms 

Immediately after ingestion the drug begins to 
dilate blood vessels throughout the body; overdose 
causes headache, flushing of skin, vomiting, diz- 
ziness, collapse, low blood pressure, coma, and 
respiratory paralysis. 

Treatment 

Induce vomiting with syrup of ipecac followed by 
activated charcoal. 
See also ergot. 

nitroprusside Sodium nitroprusside is a drug that 
dilates blood vessels typically given to treat high 
blood pressure and heart failure and to induce low 
blood pressure for certain operations. Poisoning 
may occur with one single large overdose or with 
prolonged use. It is also used in the treatment of 
stimulant or monoamine oxidase (MAO) inhibitor 
overdose. 

Poisonous part 

Nitroprusside releases free cyanide; acute cyanide 
poisoning may be produced with a high-dose infu- 
sion of nitroprusside. 

Symptoms 

The most common symptom is a rapid fall in blood 
pressure. Cyanide poisoning includes symptoms of 
headache, hyperventilation, muscle spasms, anxi- 
ety, agitation, seizures, and metabolic acidosis. 

Treatment 

In the case of cyanide poisoning, administer sodium 
thiosulfate; sodium nitrite may worsen low blood 
pressure and is not indicated. Continue to treat 
symptoms; hemodialysis may help victims with 
kidney problems. 

See also cyanide; monoamine oxidase (mao) 

INHIBITORS. 



nitrous oxide Also known as "laughing gas" 
widely used by dentists and available on college 
campuses, nitrous oxide is a general anesthetic and 
is used in a wide variety of commercial products, 
including whipped cream and cooking oil sprays. 

Discovered in 1776, it was not used as an anes- 
thetic until 23 years later; it was not widely used 
until I860. It was, however, popular at parties; Sir 
Humphry Davy, the first person to synthesize the 
gas, enjoyed nitrous oxide parties as did the poets 
Samuel Coleridge and Robert Southey, and Peter 
Roget, author of Roget's Thesaurus. Reportedly, stu- 
dents in the early 1 9th century used nitrous oxide 
for recreational purposes, and one student actually 
quit medical school and began selling the stuff for 
25? per dose. 

However, this nonflammable, nearly odorless 
gas does not produce a complete anesthesia at 
safe levels and is therefore used as a painkiller or 
together with stronger anesthetic agents. It is often 
abused for the euphoria it produces and is easily 
available on the street. 

Poisonous part 

Nitrous oxide depresses the central nervous system 
and, when used without enough oxygen, can be 
fatal. 

Symptoms 

If used improperly (that is, without sufficient oxy- 
gen), nitrous oxide can cause irregular heart patterns, 
brain damage, death, headache, cerebral edema, and 
permanent mental deficiency. Symptoms appear 
within a few seconds to several minutes. 

Treatment 

There is no specific antidote. Administer oxygen; 
give symptomatic treatment. Chronic symptoms 
should disappear between two and three months 
after exposure has ended. 

See also anesthetics, gaseous/volatile. 

nonsteroidal anti-inflammatory drugs (NSAIDs) 

This is a group of chemically diverse drugs widely 
used for the treatment of pain and inflammation. 
On their own, anti-inflammatory drugs are not 
very toxic, but victims with gastrointestinal tract 



Norwalk virus 171 



disease, peptic ulcers, or poor heart function and 
those on anticoagulant drugs should avoid them. 
Inflammation results in an increased blood flow, 
which in turn produces swelling, redness, pain, and 
heat. Inflammation is one of the body's defense 
mechanisms in response to infection and certain 
chronic diseases such as rheumatoid arthritis. 

NSAIDs include ibuprofen (Motrin, Rufen, 
Advil, Haltrain, Medipren, Nuprin), fenoprofen 
(Nalfon), meclofenamate (Meclomen), naproxen 
(Anaprox, Naprosyn), sulindac (Clinoril), indo- 
methacin (Indocin), tolmetin (Tolectin), mefanamic 
acid, piroxicam (Feldene), oxyphenbutazone, and 
phenylbutazone. 

None of these should be taken with other non- 
steroid analgesics or with warfarin or other oral 
anticoagulants, because bleeding time may be 
prolonged while on anti-inflammatory pain reliev- 
ers. Antacids, however, may sometimes reduce the 
effects of an anti-inflammatory drug. 

Symptoms 

While an overdose of most of the NSAIDs causes 
little toxicity beyond stomach pain, there are a 
few that do produce severe toxicity: oxyphenbuta- 
zone, phenylbutazone, mefenamic acid, piroxicam, 
and diflunisal. In general, symptoms appear after 
ingesting more than five to 10 times the therapeu- 
tic dose. 

If a person is allergic to aspirin or other nonste- 
roid analgesic drugs, using another anti-inflamma- 
tory medicine could be fatal. Anti-inflammatory 
drugs become toxic when given to those with kid- 
ney problems, since the kidneys can't cleanse the 
blood. Overdose causes kidney failure and severe 
liver reactions, including fatal jaundice. 

Normally NSAID overdose produces mild stom- 
ach upset, with nausea and vomiting plus abdomi- 
nal pain. Occasionally, other symptoms might 
include sleepiness, lethargy, nystagmus (an invol- 
untary oscillation of the eyeball), tinnitus (ringing 
in the ears), and disorientation. However, with the 
more toxic drugs listed above and significant over- 
dose of ibuprofen (in excess of 3,200 mg per day), 
symptoms may include seizures, coma, metabolic 
acidosis, kidney and liver failure, and cardiorespi- 
ratory arrest. Diflunisal overdose resembles salicy- 
late poisoning. 



Treatment 

There is no antidote. Maintain symptomatic treat- 
ment together with antacids for mild stomach 
problems; perform gastric lavage, followed by the 
administration of activated charcoal and a cathar- 
tic. Research suggests charcoal hemoperfusion may 
help in the treatment of phenylbutazone overdose, 
although it has not been proven. 

Norwalk virus The most common cause of viral 
contamination in shellfish is the Norwalk virus, 
which can cause food poisoning when raw or 
improperly cooked food has been in contact with 
water contaminated by human excrement. The 
disease is mild and self-limiting and usually lasts 
for one or two days. Between July 1997 and June 
2000, the Centers for Disease Control and Pre- 
vention (CDC) received 232 reports of norovirus 
outbreaks, 57 percent of which were foodborne, 
16 percent were due to person-to-person contact, 
3 percent were waterborne, and 23 percent were 
of unknown origin. The CDC estimates that 23 
million cases of acute gastroenteritis are caused by 
norovirus infection. 

Most foodborne outbreaks of the virus are likely 
to arise through direct contamination of food by a 
food handler immediately before it is consumed. 
Eating raw or poorly steamed clams and oysters 
also poses a high risk of infection. Outbreaks of 
gastroenteritis have been associated with oysters 
from contaminated waters as well. Other foods, 
including salads and raspberries, have been con- 
taminated and their consumption has resulted in 
widespread illness. 

Symptoms 

Symptoms begin one to two days after eating con- 
taminated food and include fever, weakness, appe- 
tite loss, headache, diarrhea, nausea and vomiting, 
and stomach pain. Dehydration is the most com- 
mon complication and can be especially dangerous 
for young children and the elderly. Severe illness 
is very rare. 

Treatment 

Symptomatic; replace fluids and correct electrolyte 
disturbances using oral and intravenous fluids. 



172 nutmeg 



Prevention 

Raw shellfish should be cooked for at least four 
minutes at 1 94°F. Patients with diarrhea or vomit- 
ing should not prepare food. 

nutmeg (Myristica fragrans) In small quantities 
this common spice is edible, but in large doses it 
can be fatal. Produced from the dried seeds of the 
nutmeg tree, it is found in the South Pacific and 
the East Indies. Mace, another popular spice and 
the extract used as a spray to discourage attackers, 
is also obtained from this tree. 

Nutmeg has been used since the seventh cen- 
tury A.D. to treat asthma and fever. It takes up to 
three whole nutmegs or up to 15 g of the grated 
spice to become intoxicated. 

Symptoms 

Symptoms appear within two to six hours after 
ingestion and include sedation, euphoria, and hal- 
lucinations, which can last up to two days. The 
stimulation of the central nervous system may 
be accompanied by tachycardia, skin flushing, 
decreased salivation, and delirium, with nausea, 
vomiting, and abdominal cramps. Other symp- 



NONSTEROIDAL ANTI-INFLAMMATORY DRUGS 



Drug 


Usual Daily 
Dose (adult) 


Maximum 
Recommended 
Daily Dose 
(adult) 


fenoprofen 


900-2,400 mg 


3,200 mg 


ibuprofen 


900-2,400 mg 


2,400 mg 


indomethacin 


50-150 mg 


200 mg 


meclofenamate 


200-400 mg 


400 mg 


mefenamic 


1,000 mg 


1,000 mg 


naproxen 


500-1,000 mg 


1,250 mg 


piroxicam 


20 mg 


20 mg 


sulindac 


300-400 mg 


400 mg 


tolmetin 


1,200-1,800 mg 


2,000 mg 



toms, much like those of intoxication with PCP, 
can include belligerent behavior and hyperactiv- 
ity. Occasionally, complications can lead to coma, 
shock, and death. In very high doses, nutmeg can 
cause liver damage and death. 

Treatment 

Gastric lavage; supportive treatment including a 
cathartic. Administer barbiturates or diazepam to 
control convulsions. 



nux-vomica (Strychnos nux-vomica) [Other 
names: strychnine.] Found in India and Hawaii, 
this "dog button plant" is actually a small tree, 
with oval leaves and yellow to white clusters 
of flowers. Its small, attractive fruit resembles a 
mandarin or Chinese orange and looks tempting 
to eat; the fruit contains seeds that look like gray 
velvet buttons. 

Poisonous part 

The entire tree contains strychnine, but the seeds 
contain the greatest concentration of the poison. 
The blossoms, which smell of curry powder, can be 
mistaken by a child as edible and are therefore a 
potential cause of poisoning. 

Symptoms 

Extreme irritability and restlessness followed by 
exhaustion, sweating, muscular rigidity, respira- 
tory problems, and death. In severe cases, there 
are often generalized spasms that last from a few 
seconds to several minutes and are caused by 
external sensory stimuli. Metabolic acidosis may 
also appear. 

Treatment 

Establish an airway, provide oxygen if needed; 
convulsions may call for a general anesthetic and 
muscle relaxant; reduce fever and correct acidosis 
with intravenous sodium bicarbonate. 
See also strychnine. 



o 



octopus, blue-ringed (Hapalochlaena maculosa) 

The only poisonous octopus, this small, harmless- 
looking marine animal seems playful and cute, 
but its bite can be fatal. The octopus is brown and 
speckled, with blue bands around its tentacles 
that glow just before the poison is released. Just 4 
inches long, this unique octopod is usually found 
in shallow waters around the coast of Australia and 
can be deadly if provoked. It feeds on mollusks and 
crabs with its strong beak and can commonly be 
found under rocks at low tide. 

Normally, both males and females are equally 
toxic, but when the female blue-ring begins brood- 
ing her eggs, her venom becomes even more 
potent. However, like most other female octopuses, 
she stops eating once she deposits her eggs and, 
soon after they hatch, she dies. 

A relative, the Australian spotted octopus (H. 
lunulata), lives near Queensland, New South Wales, 
Sydney, and Victoria, in the Indian Ocean, and 
Japan. Another relative, almost as deadly, is the 
North American west coast octopus (Octopus apol- 
lyon), found from Alaska to Baja California. 

Symptoms 

The bite of the blue-ringed octopus is often not 
even noticed and usually occurs when the creature 
is picked up or played with, as it is generally shy 
and stays away from humans. Immediately after 
the bite, the poison begins to affect the central 
nervous system, causing severe pain and paralyzing 
muscles of the entire body until breathing stops. Its 
poison can kill in minutes. 

Treatment 

Immediately after the bite, it is important to main- 
tain breathing through mouth-to-mouth resuscita- 



tion, since death usually occurs as a result of the 
neuromuscular poisons. 

oleander (Nerium oleander) Also known as Jeri- 
cho rose, this extremely deadly poisonous plant is a 
native of Asia and is widely cultivated in the United 
States as an ornamental shrub and houseplant. It is 
widely planted in the South and Southwest because 
of its beautiful flowers and is widely found in the 
South planted along driveways and property lines 
as a colorful hedging. This plant's toxic reputation 
has been known since ancient times, although the 
general population today may not be aware of its 
deadly properties. 

Oleander is a fragrant evergreen shrub with 
white, yellow, pink, or red blossoms and narrow 
leathery leaves that can reach 10 inches. Winged 
seeds are borne in long, narrow capsules. 

Poisonous part 

All parts of the oleander plant are poisonous; one 
leaf can kill an adult. Even the nectar from the 
flower, honey from the pollen, the smoke from the 
burning plant, and the water in which flowers are 
placed are poisonous. The clear, gummy sap con- 
tains cardiac glycosides, oldendrin and nerioside, 
which stop the heart. Serious poisoning cases have 
been reported from using oleander twigs to roast 
meat; children can be poisoned by chewing on a 
single leaf or flower. 

Symptoms 

Onset of symptoms may be immediate: pain in 
the mouth and throat, nausea, severe vomiting, 
stomach pain, bloody diarrhea, dizziness, altered 
state of consciousness, slow or irregular heartbeat. 



173 



174 oleander, yellow 



dilated pupils, drowsiness, slow respiration, coma, 
and death. 

Treatment 

Prompt gastric lavage is vital, together with cardiac 
depressants to control heart rhythm. The preferred 
antidote is dipotassium instead of calcium EDTA, 
since dipotassium chelates calcium in the body. 
Activated charcoal may be given later. Treatment is 
similar to that for digitalis poisoning. 
See also cardiac glycosides; foxglove. 

oleander, yellow (Thevetia peruviana) While its 
action is the same as that of oleander and it is just 
as poisonous, its sap is milky. Growing to 20 feet 
tall, with leaves very similar to those of oleander, 
this plant has flowers that are yellow with a hint of 
peach. The small oval fruit contains up to four flat 
seeds. Yellow oleander is found in the southwest- 
ern United States, Florida, the West Indies, Hawaii, 
and Guam. 

Poisonous part 

All parts of the oleander plant are poisonous — 
especially its seeds, which contain a glycoside simi- 
lar to digitalis. 

Symptoms 

Onset of symptoms may be immediate or appear 
later, depending on the amount of toxin ingested: 
nausea, severe vomiting, stomach pain, bloody 
diarrhea, dizziness, altered state of consciousness, 
slow or irregular heartbeat, dilated pupils, drowsi- 
ness, and slow respirations. 

Treatment 

Prompt gastric lavage is vital, followed by activated 
charcoal, together with cardiac depressants to con- 
trol heart rhythm. Treatment is similar to that for 
digitalis poisoning. 

See also cardiac glycosides; foxglove. 

olestra A fat-based substitute for conventional 
fats used in certain snack foods that, because of its 
unique chemical composition, adds no fat or calo- 
ries to food. Potato chips, crackers, tortilla chips, or 



other snacks made with olestra (Olean) are lower 
in fat and calories than snacks made with tradi- 
tional fats. 

The U.S. Food and Drug Administration (FDA) 
found that olestra may cause abdominal cramp- 
ing and loose stools in some people and that it 
inhibits the body's absorption of certain fat-soluble 
vitamins and nutrients. Products with olestra must 
carry a label stating that olestra is present and that 
the fat substitute "may cause abdominal cramping 
and loose stools. Olestra inhibits the absorption of 
some vitamins and other nutrients. Vitamins A, D, 
E and K have been added." 

The two main producers of olestra-containing 
chips, Procter and Gamble and Frito-Lay, asked the 
FDA to drop its requirement for a warning notice on 
their products, stating that there was no proof oles- 
tra caused the symptoms reported. However, more 
than 20,000 consumers had filed complaints as of 
2004, saying that olestra had caused problems rang- 
ing from gas to bloody stools to cramps so severe 
that they had to be treated in an emergency room, 
according to reports by the Center for Science in the 
Public Interest. In 2002, Procter and Gamble sold 
their factory in Cincinnati that produced olestra. 

In 2003, researchers reported two cases of 
severe gastrointestinal conditions that developed 
in previously healthy children, which appear to 
have been caused by use of olestra. In one, an 
11 -year-old girl developed cramps, flatulence, and 
foul-smelling diarrhea over two weeks while eating 
olestra chips. Although these symptoms dimin- 
ished when she stopped eating the chips, she then 
developed rectal bleeding and was found to have 
ulcerative colitis. In a 13-year-old boy, consump- 
tion of olestra chips appeared to be the cause of his 
constipation and abdominal distention, which then 
escalated into severe back pain, explosive diarrhea, 
gas, and abdominal cramps. After the boy lost 23 
pounds within a few months, most of his colon 
was removed. 



opium (Papaver somniferum) This sticky sub- 
stance is found in the fruit and juices of the opium 
poppy, which grows throughout Europe, Asia, and 
the tropics and can be combined with other drugs to 
form laudanum, paragoric, and other medications. 



organophosphate insecticides 175 



It has been used in the Orient since 200 b.c, 
when it was mentioned in the writings of Theo- 
phrastus, a Greek philosopher who studied under 
Aristotle. At that time, opium was given through 
punctures in the skin or inhaled as a vapor into the 
nose and mouth, where it unpredictably produced 
either analgesia or death. In the second century 
A.D., the Greek physician Galen was treating his 
patients with opium, and in 700 years it had spread 
to Arabia. 

In the 1 6th century, physicians figured out how 
to create laudanum from opium, but its use gradu- 
ally evolved to include recreational abuse, and by 
the late 1600s opium smoking had spread every- 
where. Opium was introduced as a medicine in 
Britain in 1680 by Thomas Syndenham, an English 
physician who proclaimed that opium was "univer- 
sal and efficacious." 

By 1729, however, its negative side was recog- 
nized in Asia, and opium smoking was outlawed 
in China and its import from India banned. Unfor- 
tunately, the British East India Company (which 
imported the drug) refused to stop and smuggled 
the drug into China — leading to the so-called 
opium wars between Great Britain and China in 
1839 and again in 1856. 

Opium's use reached a peak in popularity during 
Victorian times, when cities were honeycombed 
with opium dens and physicians prescribed lauda- 
num for a variety of "female problems" (cramps, 
menstrual distress, etc.). Its use spread to the 
United States with the thousands of Chinese labor- 
ers imported to help build the western railroads in 
the middle of the 1 9th century. 

Today, the extraction of morphine and the 
development of synthetic narcotics have rendered 
opium obsolete, and it is considered an old-fash- 
ioned remedy. It is used to treat infants who are 
born addicted because of their mothers' abuse of 
narcotics, usually in the form of paregoric, a mix- 
ture of opium, camphor, benzoic acid, and alcohol. 
Opium is classified as a Schedule II or III drug 
depending on its form. 

Symptoms 

Opium, which contains codeine, morphine, theba- 
ine, papaverine, and narcotine, is a central nervous 
system depressant that restricts pupil size, slows 



breathing, and causes nausea, vomiting, constipa- 
tion, weak pulse, low blood pressure, dehydration, 
and euphoria followed by cardiovascular depres- 
sion, unresponsiveness, coma, respiratory failure, 
and death within two to three hours of ingestion 
of a large dose. 

Treatment 

Gastric lavage followed by activated charcoal and 
cathartics, with the administration of naloxone and 
other supportive and symptomatic treatment. 
See also codeine; laudanum; morphine. 

oral contraceptives See birth control pills. 

organophosphate insecticides These extremely 
potent insecticides interfere with nerve signal 
transmission and, if ingested, can cause serious 
systemic poisoning and death. The most common 
organophosphate insecticide is parathion. An out- 
growth of nerve gas research done in Germany 
during the 1930s, these insecticides are often used 
by commercial growers to control insect pests and 
are the most common sources of insecticide poi- 
soning in humans. The Environmental Protection 
Agency has reported that more than 80 percent of 
all pesticide poisoning hospitalizations were caused 
by the organophosphates, mostly involving chil- 
dren, laborers, and farmers. 

Organophosphate insecticides like malathion 
and diazanon are also used by home gardeners to 
control spider mites, aphids, mealy bugs, and other 
pests. They continue to be popular because they 
are effective and don't remain in body tissues or 
the environment, due to their unstable chemical 
structure that disintegrates into harmless radicals 
within days of application. The organophosphates 
have largely replaced banned DDT as an agricul- 
tural insecticide. 

Still, the use of organophosphate pesticides 
can result in a buildup of residue on leaves 
and stems and — if used inside the home — can 
result in the release of noxious vapor into the 
air. Individual organophosphates vary widely in 
their toxicity; probably the most dangerous is 
TEPP (tetraethylpyrophosphate), the oldest known 



176 oven cleaner 



organophosphate; malathion lies at the other end 
of the spectrum as the least toxic of the group. 

The organophosphates interfere with the enzyme 
cholinesterase, which helps to regulate the amount 
of acetylcholine in the body; this causes a buildup 
of acetylcholine, which interferes with the central 
nervous system and the parasympathetic nervous 
system. 

Toxic levels of organophosphates occur in chil- 
dren who ingest pesticides or animal flea and tick 
killers; they also occur in agricultural exposure 
by farm workers and suicide attempts (the largest 
number of cases). 

For those occupations involving exposure to 
organophosphates, such as factory workers pro- 
ducing lubricants, fire retardants, and pesticides, it 
should be understood that these compounds are 
highly toxic and can penetrate the skin without pro- 
ducing sensations and can be fatal. These compounds 
are being investigated for delayed neurotoxicity. 

Symptoms 

Symptoms usually appear within 24 hours of expo- 
sure but vary according to the specific chemical, 
exposure and type of contamination. At first, symp- 
toms include headache, cramps, vomiting, diarrhea, 
dizziness, weakness, sweating, and salivation. In 
cases of severe poisoning, symptoms include coma, 
pulmonary edema, psychosis, convulsions, brady- 
cardia, cyanosis, twitching, and paralysis. Death 
usually occurs within 24 hours after complications 
occur in cases that have not been treated, or within 
10 days in treated cases. 

Treatment 

Remove all contaminated clothes, wash thoroughly 
with soap followed by a second wash with alcohol. 
Administer syrup of ipecac (if victim is fully alert) 
and perform gastric lavage. Atropine is the antidote 
for organophosphate poisoning, with the possible 
administration of pralidoxime. 
See also DDT; malathion; TEPP. 

oven cleaner See alkaline corrosives. 

oxalates A class of compounds related to oxalic 
acid, named after the wood sorrel (Oxahdaceae) 



family, in which it was first identified. Oxalate 
salts and oxalic acid are found in philodendron, 
dieffenbachia, and other plants and can be very 
irritating to the skin and mucous membranes. In 
severe cases, exposure to calcium oxalate can cause 
the throat to swell shut, resulting in suffocation. In 
addition, oxalic acid and many of the oxalate salts 
can become concentrated in the kidneys and cause 
systemic poisoning. 

See also dieffenbachia; philodendron. 

oxycodone A semisynthetic derivative of codeine 
marketed in the United States in liquid, tablet, 
extended-release tablet, capsule, and concentrated 
solution form. OxyContin is perhaps the most well- 
known form of this narcotic. Oxycodone is also an 
ingredient in many combination products, appear- 
ing with acetaminophen (Endocet, Percocet, and 
others), aspirin (Endodan, Percodan, Roxiprin, and 
others), and ibuprofen (Combunox). Oxycodone 
is a Schedule II drug (drug with high potential for 
abuse) capable of inducing a morphine-like depen- 
dence stronger than that associated with codeine. It 
has about the same painkilling ability as morphine 
when injected, and it retains half of its effectiveness 
when given by mouth. 

Symptoms 

Respiratory depression, stupor, cold and clammy 
skin, slow heartbeat, and low blood pressure. More 
severe overdoses can lead to apnea, circulatory col- 
lapse, coma, cardiac arrest, and death. 

Treatment 

The antidote is naloxone. Do not induce vomiting. 
Gastric lavage may be effective even after several 
hours following ingestion; administer activated 
charcoal and a saline cathartic. Give supportive and 
symptomatic treatment; seizures may be controlled 
with intravenous diazepam (Vahum). 

See also codeine; morphine; naloxone; narcot- 
ics; Percodan. 



oxygen This colorless, odorless gas is essential for 
all forms of life on earth, because it is necessary for 
the metabolic burning of foods to produce energy 



oxymorphone 177 



(aerobic metabolism). Oxygen is also used as a 
treatment following inhalation of toxic gases; 100 
percent oxygen is indicated for carbon monoxide 
poisoning; hyperbaric oxygen (100 percent oxygen 
delivered to the victim in a pressurized chamber) is 
believed by some experts to more rapidly improve 
recovery from carbon monoxide poisoning. 
See also carbon monoxide poisoning. 



oxymorphone A semisynthetic derivative of oxy- 
codone and a narcotic painkiller, oxymorphone has 
less of a depressing effect on the cough reflex; it is 
therefore used primarily as a painkiller for postsur- 
gical patients. Reported to be more than 10 times 
stronger than morphine and almost twice as toxic, 
it is equally addictive. 



Symptoms 

Respiratory depression, stupor, cold and clammy 
skin, slow heartbeat, and low blood pressure. More 
severe overdoses can lead to apnea, circulatory col- 
lapse, coma, cardiac arrest, and death. 

Treatment 

The antidote is naloxone. Do not induce vomiting. 
Gastric lavage may be effective even after several 
hours following ingestion; administer activated 
charcoal and a saline cathartic. Give supportive and 
symptomatic treatment; seizures may be controlled 
with intravenous diazepam (Vahum). 

See also morphine; naloxone; narcotics; 

OXYCODONE. 



p 



paint removers See hydrocarbon. 

paint thinner See petroleum distillates. 

panther mushroom (Amanita pantherina) Often 
confused witfi its close relative, fly agaric, the pan- 
tfier mushroom is a relatively small, squat plant 
with a cap surface colored from yellow to purple- 
brown and covered with white warts. Raised in the 
United States, it is found in spring and fall in conifer 
woods west of the Cascade Mountains in Oregon 
and Washington. 

Poisonous part 

Muscimol is a water-soluble toxin first isolated in 
the early 1960s from both the fly agaric and the 
panther mushroom. Both muscimol and its meta- 
bolic precursor, ibotenic acid, are believed to be the 
primary cause for the toxicity of these two mush- 
rooms and a few related species. 

Symptoms 

Deaths from eating the panther mushroom have 
occasionally been reported in the United States. 
Within 20 to 90 minutes after ingestion, muscimol 
begins to affect the central nervous system, causing 
drowsiness, stupor, elation, hyperactivity, delirium, 
confusion, hallucinations, heartbeat problems, 
gastroenteritis, urinary retention, blurred vision, 
watery diarrhea, and convulsions. 

Treatment 

Induce vomiting and perform gastric lavage; admin- 
istration of physostigmine and diazepam (Valium) 
may help control symptoms and convulsions. 
Stimulants are not advised. 



See also Amanita mushrooms; fly agaric; mus- 
cimol; MUSHROOM poisoning; mushroom toxins. 

paradichlorobenzene One of two common 
ingredients in mothballs and toilet bowl cleaners 
(the other is naphthalene), this chemical has a 
pungent odor but is far less toxic than naphtha- 
lene. However, ingestion of large amounts can still 
cause stomach upset and central nervous system 
stimulation. Up to 20 grams have been well toler- 
ated by adults. 

Symptoms 

Nausea and vomiting very soon after ingestion. 
Treatment 

There is no specific antidote. Administer activated 
charcoal and a cathartic. Treat coma or seizures if 
they occur. 

See also naphthalene. 



paralytic shellfish poisoning (PSP) The most seri- 
ous of all four forms of shellfish poisoning caused 
by toxic forms of plankton that produce a deadly 
neurotoxin (saxitoxin). Most cases of PSP have 
occurred when people ate raw tainted shellfish, 
although cooking will not destroy the toxin. 

An incidence of PSP was recorded as early as 
1689, and further outbreaks have been recorded 
many times since then. Traditionally, it has been 
considered a danger only to shellfish harvested 
in cold water, but the rate of incidence in tropical 
areas has been increasing. Oysters, clams, cockles 
and mussels are particularly prone to contamina- 
tion because of their metabolic system, which 
pumps water across the gills to isolate plankton for 



178 



parasympathomimetic drugs 179 



their food. Crustacean shellfish (such as lobsters) 
only very rarely transmit PSP. In mussel, toxins 
are concentrated in the digestive glands and toxic- 
ity is usually lost within weeks, but the Alaskan 
butter clam can remain toxic for up to two years. 
However, the part of the mollusk that humans gen- 
erally eat — the white meat, without the digestive 
glands — stores fairly small amounts of toxin. 

Symptoms 

Signs of shellfish poisoning develop within five to 
30 minutes after eating contaminated crabs, clams, 
or mussels. Symptoms include gradual paralysis 
and trembling, with nausea, vomiting, and diar- 
rhea. Later on, there may be shortness of breath, 
dry mouth, choking feeling, confused or slurred 
speech, and lack of coordination. Eating even a tiny 
amount of contaminated shellfish can be fatal, and 
survival usually depends on how much has been 
consumed. 

Treatment 

There is no known antidote for shellfish poison- 
ing caused by saxitoxin, and no drug has proven 
effective, so treatment is supportive for infected 
patients. CPR may be needed as first aid. If the vic- 
tim survives the first 12 hours, prognosis for com- 
plete recovery (within a few days to two weeks) is 
good; however, between 8 and 23 percent of PSP 
poisonings are fatal. 

Prevention 

You can't tell just by looking at the water whether 
toxic plankton are present. If you're not sure if the 
seafood you're eating is toxin-free, avoid eating it. 
To prevent outbreaks, samples of susceptible shell- 
fish are tested for toxin by state health departments 
during certain times of the year. If contamination 
is found, affected growing areas are quarantined, 
and sale of shellfish prohibited. Warning signs are 
posted in shellfish growing areas, on beaches, and 
in the news. Fish and shellfish sold for human 
consumption must meet Food and Drug Adminis- 
tration standards of less than 80 micrograms of PSP 
toxin per 100 grams of shellfish tissue. You can't 
eliminate PSP from shellfish by cooking or freez- 
ing; even when pressure-cooked at 250°F for 15 
minutes, it remains toxic. 



Paraquat This powerful defoliant is not gener- 
ally available on store shelves, as it can be toxic 
if inhaled, absorbed through the skin or ingested. 
Diquat, which is only half as toxic as Paraquat, is 
used much more widely as a defoliant; the two are 
contained together in a 2.5 percent granular for- 
mulation known as Weedol. 

Solutions available for home use are generally 
extremely dilute (0.2 percent), but the commercial 
varieties may contain up to 21 percent Paraquat. 

Symptoms 

Appearing two to five days after ingestion, symp- 
toms include burning mouth and throat, vomiting, 
abdominal pain, swelling, diarrhea, and fever. This 
is followed by liver and kidney damage and then 
respiratory problems, cyanosis, and fatal lung dete- 
rioration. Ingestion of as little as two to four grams 
(or 10 to 20 milliliters of concentrated 20 percent 
solution) has been fatal. Food in the stomach 
may bind Paraquat, preventing its absorption and 
reducing its toxicity. 

Poisoning with Diquat may cause corrosive 
injury, with severe gastroenteritis, massive fluid 
loss, and kidney failure. 

Treatment 

There is no specific antidote. Induce vomiting 
with syrup of ipecac if gastric lavage is not possible 
or activated charcoal is not available (carefully, 
as paraquat can be corrosive). Immediately after 
vomiting, administer absorbent clay (or activated 
charcoal if clays are not available) plus a cathartic. 
Ingestion of any food or even plain dirt may give 
some protection if other absorbents are not imme- 
diately available. For skin contamination, remove 
clothes and wash thoroughly; in the event of eye 
contamination, wash eyes for 15 minutes and see 
an ophthalmologist. Avoid giving excessive oxygen 
and treat fluid and electrolyte imbalances. 
See also herbicides. 



parasympathomimetic drugs These drugs, includ- 
ing physostigmine, pilocarpine, neostigmine, and 
methacholine, act on the parasympathetic nervous 
system and are administered by ingestion, injec- 
tion, or application to mucous membranes. They 



180 parathion 



are used to treat glaucoma, myasthenia gravis, 
bladder problems, and certain heart irregularities. 

Symptoms 

Overdose produces breathing problems, tremor, 
involuntary defecation and urination, pinpoint 
pupils, vomiting, low blood pressure, bronchial 
constriction, wheezing, twitching, fainting, slow 
pulse, convulsions, and death. Repeated small 
doses may mimic symptoms of acute poisoning. 

Treatment 

Prompt administration of atropine results in imme- 
diate recovery. 

See also physostigmine. 

parathion (0,0-diethyl 0-p-nitrophenyl phospho- 
rothioate) This brown-yellow liquid is used as 
an insecticide and also as a deadly nerve gas that 
is fatal upon contact. Most fatalities have occurred 
while spraying into the wind, cleaning equipment 
(and airplanes) used for spraying, or gathering pro- 
duce that has been sprayed. Industrial poisonings 
have also occurred by workers who absorb the poi- 
son through the skin. It is also a common suicide 
choice in Europe. 

Poisonous part 

The toxic compound includes muscarine and other 
poisonous substances that have not yet been fully 
identified. 

Symptoms 

Parathion is highly toxic by skin contact, inhala- 
tion, or ingestion. It destroys enzymes needed 
for proper functioning of nerves and muscles, 
causing contraction of pupils, headache, sensitiv- 
ity to light, spasms, abdominal pain, nosebleeds, 
nausea, muscle weakness, twitching, diarrhea, 
convulsions, heart block, paralysis, respiratory 
difficulty, and pulmonary edema, ending in fatal 
respiratory failure. Death is usually quite painful, 
with tremors, muscle spasms, and convulsions. 
Parathion used as a nerve gas is fatal upon skin 
contact, although it can also be absorbed by the 
lungs; it causes painful tremors, muscle spasms, 
convulsions, and death. 



Treatment 

The antidote is large doses of atropine for 48 hours 
plus treatment of symptoms. 

See also muscarine; organophosphate insec- 
ticides. 



pavulon (pancuronium) See neuromuscular 

BLOCKING AGENTS. 



PCBs See polychlorinated biphenyls. 



PCP See PHENCYCLIDINE. 



peach pit See Prunus. 

penicillamine One of the derivatives of penicil- 
lin used not for fighting microbes, but for binding 
and removing heavy metals such as lead, mercury, 
arsenic, and copper from the body. It is often used 
following an initial treatment with calcium EDTA 
or dimercaprol. Penicillamine is easily absorbed in 
the body; the penicillamine and metal can then be 
excreted from the body. 

See also arsenic; calcium EDTA; dimercaprol. 



pennyroyal oil A volatile oil obtained from the 
pennyroyal plant (Mentha pulegium), one of a large 
number of plants belonging to the mint family. 
Pennyroyal has traditionally been used by Ameri- 
can Indians to bring on menstrual periods and to 
cause abortions. A colorless liquid, pennyroyal oil 
readily evaporates at room temperature. 

Symptoms 

In large doses, pennyroyal oil induces a fatal reac- 
tion as a result of kidney failure. 

Treatment 

There is no known antidote for pennyroyal oil. 
Treatment is supportive and symptomatic. 
See also volatile oils. 



persistent organic pollutants 181 



pep pills See amphetamines. 

Percodan (oxycodone) This narcotic painkiller 
derived from morphine is used in the treatment of 
severe pain and is a combination of oxycodone and 
aspirin. Percodan depresses the central nervous 
system and its sedative qualities are strengthened 
when taken together with tranquilizers, antihis- 
tamines, antidepressants, sedatives, sleeping pills, 
alcohol, or narcotics. Combining this drug with 
phenytoin (Dilantin) can cause brain death. 

Symptoms 

When Percodan is taken in overdose, symptoms 
include drowsiness, clumsiness, lightheadedness, 
dizziness, sedation, nausea, and vomiting; severe 
overdose can produce weak muscles, stupor, coma, 
low blood pressure, respiratory depression, and 
cardiac arrest within 30 minutes. 

Treatment 

The antidote is naloxone. 

See also morphine; naloxone; narcotics; oxy- 
morphone; phenytoin. 

persistent organic pollutants POPs, or persistent 
organic pollutants, are a group of toxic chemicals 
that persist in the environment for long periods of 
time, and which biomagnify (increase in concen- 
tration, often to dangerous levels) as they move 
up the food chain. Persistent organic pollutants 
are often released into the environment through 
industrial, agricultural, and other human activities 
and carried around the world through the atmo- 
sphere, oceans, and other pathways, far away from 
their originating point. Because of their chemical 
makeup, POPs accumulate in fatty tissue in both 
humans and animals, including fish, fowl, meat, 
and dairy products. This global contamination 
process, along with the fact that POPs are associ- 
ated with various harmful effects on human and 
animal health, including cancer, nervous system 
damage, reproductive disorders, and disruption of 
the immune system, prompted countries to begin 
limiting the production, use, and release of POPs 
into the environment. What started out as local 



and then regional efforts soon became a global 
one, and the Stockholm Convention was created 
on May 22, 2001. This was a legally binding agree- 
ment, originally signed by 150 countries, entered 
into force in May 2004, and had 120 parties as part 
of the agreement as of March 2006. 

The Convention on Persistent Organic Pollut- 
ants, which was signed by the United States in May 
2001, is a commitment to reduce and/or eliminate 
the use, production, and/or release of the twelve 
POPs that are of the greatest concern to the world. 
The twelve POPs (known as the "dirty dozen") 
include aldrin, chlordane, DDT, dieldrin, endrin, 
heptachlor, hexachlorobenzene, mirex, poly- 
chlorinated biphenyls, polychlorinated dibenzo- 
p-dioxins, polychlorinated dibenzo-p-furans, and 
toxaphene. 

There are three classifications of POPS based 
on how they enter the environment. Insecticides 
are purposefully introduced into the environment. 
Although most of the POPs have been banned, 
some developing countries still use them. Indus- 
trial chemicals, such as polychlorinated biphenyls 
(PCBs) leak into the environment, while the third 
category is by-products of manufacturing and com- 
bustion and enter the air, water, and soil through 
various means. 

Symptoms 

Certain POPs can result in a disease called por- 
phyria, which may cause seizures. POPs may also 
increase the risk of infection and cancer, repro- 
ductive disorders, skin lesions, and disturbances 
in growth and development. Acute exposure to 
aldrin, dieldrin, and endrin can cause severe sei- 
zures, headache, nausea, anorexia, muscle twitch- 
ing, and psychological illnesses, and possibly 
peripheral neuropathy and death. DDT can cause 
nausea and headache, irritation of mucous mem- 
branes, tremors, and other nervous system abnor- 
malities. Heptachlor often causes hyperexcitation 
of the central nervous system, cerebrovascular 
disease, and death. Dioxins and furans reduce tes- 
tosterone levels in males, and fetuses exposed to 
dioxins through the placenta and babies through 
breast milk exhibit dysfunctional muscle reflexes, 
while infants exposed to hexochlorobenzenes often 
develop arthritis and rashes. 



182 pesticides 



Treatment 

There is no way to eliminate POPs from the 
body. Treatment is supportive and symptomatic. 
If ingested, induce vomiting or perform gastric 
lavage followed by the administration of activated 
charcoal and a cathartic. If the skin has been con- 
taminated, wash thoroughly. 

See also aldrin; dieldrin; mirex; polychlori- 

NATED BIPHENYLS; TOXAPHENE. 

pesticides Also known as "crop protectants," pes- 
ticides are chemicals used in protecting crops from 
predators, competitors, and diseases that can cause 
major losses. Specific types of pesticides are used 
for different purposes: Insecticides control insects; 
fungicides control plant diseases; herbicides control 
weeds that compete with crops; and rodenticides 
control rodents that attack crops in storage. 

American farmers use about 77 percent of 
all the pesticides in the United States, and these 
applications have a direct impact on the food sup- 
ply. The remaining 23 percent is also important, 
however. In fact, 10 percent of the land area in 
the United States (including lawns, forests, and 
parks) is treated with pesticides. It's been estimated 
that the average homeowner in the United States 
uses two to six times more pesticides per acre than 
do farmers. Runoff from all pesticide use, includ- 
ing agricultural, industrial, and personal, has the 
potential to contaminate water and soil. 

Various studies show a correlation between pes- 
ticide use and the development of cancer. In the 
Agricultural Health Study (American Journal of Epi- 
demiology, 2003), for example, researchers found an 
association between use of agricultural pesticides 
and the risk of prostate cancer. A link between pes- 
ticide use and breast cancer has been reported by 
several research studies, including a 2007 study in 
the American Journal of Epidemiology, which was the 
first to suggest that self-reported use of residential 
pesticides may increase the risk of breast cancer. 

Pesticide contamination on domestic and 
imported produce is monitored by the Food and 
Drug Administration (FDA) by testing selected 
samples. In 2003, the FDA tested 2,344 domes- 
tic and 4,890 imported produce items and found 
no residues in 62.7 percent of the domestic and 



71.8 percent of the imported samples. Only 2.4 
percent of domestic and 6.1 percent of imported 
samples had residue levels that violated the FDA's 
standards. 

Acceptable levels of pesticides are set by the 
Environmental Protection Agency (EPA), based 
on current knowledge of the long-term effects of 
pesticide residues. 

The alternative to buying conventionally grown 
produce (which has been treated with pesticides) 
is to buy organic food. For many years, the terms 
"organic" and "certified organic" had no federal 
legal definition, and organic farmers raised an out- 
cry against the lack of national standards and the 
permissive rules that applied to organic foods. In 
1998, for example, the United States Department 
of Agriculture (USDA) had proposed that food 
could be labeled "organic" even if it was irradiated 
to kill germs, genetically engineered, or subjected 
to sewage sludge or chemical sprays. These propos- 
als were withdrawn by the USDA, and new rules 
were eventually put into effect. 

Since 2002, organic certification in the United 
States has taken place under the authority of the 
USDA National Organic Program, which accredits 
organic certifying agencies and oversees the regu- 
latory process. "Certified organic" refers to agricul- 
tural products that have been grown and processed 
according to uniform standards that are verified by 
independent state or private organizations, all of 
which must be accredited by the USDA. Anyone 
who sells products labeled or marketed as "organic" 
is required by law to be certified. For a farm to be 
certified, it must submit an organic system plan 
annually and submit to inspection of the fields and 
processing facilities. Inspectors verify that the farm 
is engaging in organic practices such as long-term 
soil management and buffering between organic 
farms and nearby conventional farms. Certified 
organic requires complete elimination of synthetic 
agrochemicals, irradiation, and genetically engi- 
neered foods or ingredients. 

Rather than use pesticides, herbicides, fun- 
gicides, and other synthetic means to control 
diseases and pests, organic farmers build healthy 
soils by planting cover crops, using compost, and 
biologically based soil amendments. They use crop 
rotation, mechanical tillage, hand-weeding, cover 



pesticides, safety 183 



crops, mulches, and other management methods to 
control weeds. Pests are controlled using beneficial 
insects, birds, soil organisms, traps, and barriers. 
As a last resort, certain botanical or other nonsyn- 
thetic pesticides can be used, as approved under 
the National Organic Program Rule. 

Approximately 2 percent of the U.S. food supply 
is produced using organic methods. Since the mid 
1990s, sales of organic products have increased 
annually by at least 20 percent. In 2005, retail sales 
of organic foods and beverages were about $12.8 
billion, according to the Natural Marketing Insti- 
tute (Health & Wellness Trends Database, March 
2006). The Organic Farming Research Foundation 
reported that by 2007, there were approximately 
13,000 certified organic producers in the United 
States. Organic foods are also becoming popular in 
foreign markets, with countries like Germany and 
Japan becoming important organic food markets. 

See also Alar; aldicarb; aldrin; Bacillus 

THURINGIENSIS (BT); BENZENE HEXACHLORIDE; BOTANIC 

insecticides; carbamate; carbaryl; chlordane; 
chlorinated hydrocarbon pesticides; chloroben- 

ZENE DERIVATIVES; CREOSOTE; DDT; DERRIS; DIELDRIN; 

endrin; ethylene dibromide; indane derivatives; 
inorganic chemical insecticides; insecticides; lin- 
DANE; malathion; TEPP; toxaphene. 

pesticides, safety Some of the most common 
poisoning problems are pesticides. According to 
the National Ag Safety Database (NASD), half the 
pesticide-related deaths in the United States are 
of children under the age of 10. Almost half of all 
households with children under age five have at 
least one pesticide stored in an unlocked cabinet 
less than four feet off the ground, according to 
a survey by the U.S. Environmental Protection 
Agency (EPA). The survey also found that 75 per- 
cent of households without children under age five 
also stored one pesticide within reach of children. 
This statistic matters because research shows that 
13 percent of all pesticide poisonings occur away 
from the child's home. 

Storing pesticides 

Here are some quick and easy steps you can take to 
make sure you are storing your pesticides safely: 



• Always store pesticides in a locked cabinet or 
garden shed away from a child's reach. 

• Read the label before you use pesticides and fol- 
low all instructions, including precautions and 
restrictions. 

• Before you apply indoor or outdoor pesticides, 
be sure there are no children or toys in the area: 
keep them away until the surfaces are dry (or 
until a recommended time has passed). 

• Never leave pesticides out and open while 
you are using them (not even for a minute or 
two). 

• Never put pesticides into another container; a 
child may think there is something to eat or 
drink in the container. 

• Close the container tightly after you are finished 
using it. 

• Make sure your child's other caregivers, grand- 
parents, and so on follow these guidelines too. 

Using pesticides safely 

It is important not only to store your pesticides 
safely but to know how to use them properly as 
well. Follow these guidelines when using poten- 
tially toxic pesticide products: 

• Always read the label before you use the product 
and follow the directions. 

• Do not smoke while spraying or dusting; many 
of these chemicals are flammable. 

• Wear protective clothing and masks. Keep your 
sleeves rolled down and your collar up. 

• Wash immediately with soap and water if you 
spill pesticide material on your skin. 

• Wash your hands immediately after spraying or 
dusting and before eating or smoking. Change 
your clothes as well. 

• If you begin to feel sick while using a pesti- 
cide (or shortly thereafter), call your doctor 
immediately. 

• Investigate organic alternatives: if you do use 
toxic pesticides, hmit use and provide adequate 
ventilation. Keep children away from treated 
areas. 



184 petroleum distillates 



• If you use a bug bomb, keep children out of the 
treated area at least overnight and scrub areas 
where fumes may have settled. 

• When treating your lawn with chemicals, close 
windows and keep your child indoors until treat- 
ment is over. 

• Do not allow your child to play on chemically 
treated lawns at least until the chemicals have 
had a chance to seep into the soil; rain or a sprin- 
ging from your hose will speed this process. 

petroleum distillates A wide range of prod- 
ucts are distilled from petroleum, including paint 
thinner, kerosene, gasoline, lighter fluid, petro- 
leum-based insecticides, and mineral seal oils. All 
petroleum distillates are hydrocarbons, but not all 
hydrocarbons are petroleum distillates. Petroleum 
distillates are a specific type of hydrocarbons called 
aliphatics. 

Ingestion of large amounts of hydrocarbons 
by young children is not common because these 
chemicals have a very foul taste. Aspiration also is 
usually unintentional. Among adolescents, how- 
ever, aspiration of hydrocarbons ("huffing") is typi- 
cally done to get high. 

Between 1997 and 1999, an estimated 6,400 
children younger than five years of age were seen 
in hospital emergency departments after they acci- 
dentally ingested hydrocarbons, with petroleum 
distillates being the most common ones taken. In 
1998, unintentional ingestion of hydrocarbons 
caused the death of four children younger than 1 3 
years of age and another 14 deaths by intentional 
ingestion. 

Symptoms 

Petroleum distillates in small doses cause nausea 
and vomiting, coughing, and spitting blood. Larger 
amounts can result in weakness, dizziness, slow, 
shallow breathing, and unconsciousness followed 
by convulsions and, sometimes, mild heart attack. 
Death from ingesting petroleum distillates is almost 
always a result of pulmonary problems. 

Treatment 

Gastric lavage only when preceded by insertion 
of endotracheal tube in comatose patients. Do 



not induce vomiting (unless an insecticide or other 
poison also has been ingested with the petroleum 
distillate). The victim's head should be kept lower 
than the hips to prevent vomitus from being aspi- 
rated into the lungs. Magnesium or sodium sulfate 
or citrate may be used as a cathartic. Oxygen and 
supportive therapy may also be needed. 
See also insecticides; turpentine. 

pets, poisoning Pets are just as much at risk 
for common household poisoning as any curious 
two-year-old; curious pets can push and paw open 
cabinets, chew through child protective caps, and 
ingest toxic liquids in a very short time. Gener- 
ally, any products that are considered poisonous 
to a young child should also be locked away from 
pets, including medications, household and garden 
chemicals, insect and rat killers, and automotive 
products. 

According to experts at the National Animal Poi- 
son Control Center, it takes only a small amount of 
a potentially toxic substance to do serious harm to 
a pet. For example, one extra -strength acetamino- 
phen tablet or one teaspoon of undiluted antifreeze 
can kill a seven-pound cat. An animal's medicine 
should never be given to another species (cat medi- 
cine for dogs, and vice versa). Flea and tick prod- 
ucts can be toxic if used incorrectly, especially on 
cats, who are extremely sensitive to whole -house 
flea and tick treatments. 

Among other common products that are poison- 
ous is chocolate, which is toxic to dogs if eaten in 
sufficient quantities. Unsweetened baking choco- 
late is the most dangerous of all chocolate, as it 
contains 10 times the amount of theobromine and 
caffeine as white or milk chocolate. About one 
ounce of baking chocolate can be fatal to a ID- 
pound dog (or about one-fourth of an ounce for 
every two point two pounds). Although vomiting 
is the most common symptom, poisoning in ani- 
mals may also cause diarrhea, anorexia, or sudden 
behavior change (such as depression). According 
to veterinarians at the National Animal Poison 
Control Center, if the pet has not ingested a caustic 
or oily substance, the best emergency treatment is 
to induce vomiting. But because vomiting on an 
empty stomach will make the animal retch with- 



pets, poisoning 185 



out bringing up the toxic substance, owners should 
feed the pet a soft diet (such as canned pet food or 
milk) before giving an emetic. Possible emetics for 
pets can include syrup of ipecac, saline, or hydro- 
gen peroxide. 

A recent episode of massive pet poisoning 
occurred in 2007 and became evident early in 
the year when hundreds, and then thousands of 
dogs and cats in North America fell ill and died 
after eating contaminated pet food. The origi- 
nating contamination point was the suppHers of 
wheat gluten and rice protein concentrate from 
China, which was then used in hundreds of dif- 
ferent name brand pet foods. The first pet food 
recall began on March 16, 2007, and ultimately 
more than 130 different brand name pet foods 
for dogs and cats were pulled from the shelves as 
experts from the Food and Drug Administration 
(FDA), the American Association of Veterinary 
Laboratory Diagnosticians, experts from various 
veterinary schools, and others investigated the 
deaths. Experts believe that the contaminant 
was composed of two closely related chemi- 
cals — melamine and cyanuric acid, which then 
combined to form crystals in the kidneys of some 
animals. The crystals then blocked the microtu- 
bules through which urine flows, causing kidney 
damage, kidney failure, and sometimes death. 
The FDA reported that it appears the melamine 
was deliberately added to the ingredients in 
China to make them look like they were more 
protein-rich than they actually were. 

It is difficult to know exactly how many ani- 
mals were affected and died from the contam- 
inated food. Many veterinarians reported that 
more cats than dogs were being brought to their 
clinics, which could be explained by the fact that 
cats' well-known susceptibility to kidney problems 
places them at higher risk for kidney damage than 
dogs. Because cats evolved in the African desert 
and got all their water from their prey rather than 
from drinking, they have the unique ability to 
highly concentrate their urine. Cats' kidneys are 
thus less adept at filtering out potentially danger- 
ous waste, and they have too little water in their 
kidneys to dissolve the crystals. Dogs, however, 
drink more water and urinate more often, which 
helps them ehminate the crystals. 



If you suspect poisoning 

If your pet has ingested something that you suspect 
is toxic, call a veterinarian; do not wait for signs 
to develop. For poison treatment to be successful, 
immediate action is necessary, as many antidotes 
must be administered within 12 hours of toxin 
ingestion. If possible, bring a sample of the suspect 
substance with you to the veterinarian. Frequently 
veterinarians prescribe giving the animal one table- 
spoon of hydrogen peroxide to induce vomiting, so 
it is recommended to keep a bottle handy for emer- 
gencies. However, do not induce vomiting without 
first talking with a trained professional, as many 
chemicals (e.g., gasoline, kerosene) should not be 
eliminated through vomiting. If local expert help 
is unavailable, you may call the Animal Poison 
Control Center 24 hours a day for advice. Dial 888- 
426-4435 at a cost of $60 for a consultation fee. 

Measures to Protect Your Pets against Poisoning 

• Keep all prescription and over-the-counter 
medications out of your pets' reach. This also 
includes vitamins, herbs, and other natural 
supplements. 

• Frequently check your vehicles for antifreeze 
and windshield wiper fluid leaks. These sub- 
stances taste sweet and can be lethal in very 
small amounts to animals. Consider using ani- 
mal-friendly antifreeze products that use propyl- 
ene glycol instead of ethylene glycol. 

• If you treat your garden or lawn with fertilizers 
or pesticides, do not let your pets have access to 
these areas until they have dried completely. If 
you are uncertain about the safety of any prod- 
uct, consult your veterinarian. Always store such 
items safely away from pets. 

• Be aware of the plants you have in and around 
your home. Azalea, foxglove, laurel, oleander, 
easter lily, and many other plant species can be 
deadly if ingested. 

• If you use any type of rodent or other pest con- 
trol traps, place them in areas that are not acces- 
sible to your pets. Some traps contain ingredients 
that are very attractive to pets. 

• Use pet products as instructed on the package 
or by your veterinarian. Failing to follow usage 



186 phencyclidine 



directions is one of the most common causes of 
pet toxicity. 

• Do not give certain foods to your pets: alcofiol, 
apple seeds, apricot pits, avocados (toxic to birds, 
mice, rabbits, horses, dairy goats), chocolate, 
coffee, grapes, macadamia nuts, moldy food, 
mushrooms, onions, potato leaves and stems, 
raisins, rhubarb leaves, salt, tea, tomato leaves 
and stems, walnuts, yeast dough. 

• Secure your trashcans. Mixing food scraps with 
other waste items can be very toxic to rummag- 
ing animals. 

phencyclidine (PCP) This former veterinary drug 
became popular as a cheap street drug during the 
late 1960s, when it was widely known as "angel 
dust." It may be snorted, smoked, ingested, or 
injected and is often substituted for other illicit 
drugs such as THC (tetrahydrocannabinol, the 
active ingredient in marijuana), mescaline, or LSD. 
It produces a dissociative state and inhibits pain 
perception in its street dosage of I - to 6-milligram 
tablets; ingestion of 6 to 10 milhgrams causes toxic 
psychosis. Overdose (150 to 200 milligrams) is fatal. 
Although classified as a stimulant, PCP can both 
excite and depress the central nervous system. 

During 2003, a total of 785 exposures to phen- 
cyclidine were reported to the U.S. Poison Control 
Centers, which included eight deaths and 83 people 
who experienced severe morbidity. In that same 
year, the Drug Abuse Warning Network found 
that PCP was involved in nearly 0.75 percent of all 
drug-related emergency department visits (4,581 of 
a total of 627,923). 

PCP was developed in 1957 as an analgesic and 
short-acting intravenous anesthetic, but the side 
effects were so toxic that the drug was withdrawn 
for human use; it was later reintroduced in 1967 
only to veterinarians as an anesthetic under the 
trade name Sernyl or Sernylan. It became popular 
in the late sixties and was mixed with THC, LSD, 
psilocybin or mescaline. PCP is sprinkled onto 
parsley or marijuana for recreational smoking. 
There have been reports that users have been 
able to snap out of handcuffs and have attacked 
large groups of people and the police unarmed. 
The loss of fear may cause individuals to try to 



stop a train by standing in front of it or mutilating 
themselves. 

Symptoms 

Mild use produces lethargy, euphoria, hallucina- 
tions, and sometimes bizarre or violent behavior, 
with rapid swings between quietness and agita- 
tion. Severe overdose leads to high blood pressure, 
rigidity, high fever, rapid heartbeat, convulsions, 
and coma; the pupils are often small, and death 
may occur as a result of self-destructive behavior 
or as a result of high fever (kidney failure or brain 
damage). 

Treatment 

There is no specific antidote. Ammonium chloride 
is sometimes given to help remove the PCP from 
the central nervous system. Provide symptomatic 
treatment and sedation (benzodiazepines) to con- 
trol agitated behavior; phenothiazines and other 
antipsychotics are ineffective and may induce low 
blood pressure or seizures. Do not induce vomit- 
ing because of the risk of rapid onset of seizures 
or coma. Perform gastric lavage only if ingestion 
has occurred during the past four hours, or when 
multiple agents have been ingested. Follow by acti- 
vated charcoal and a cathartic. Mildly intoxicated 
persons should be managed with sensory isolation 
in a physically protected environment. Symptoms 
may last for several days as the drug empties into 
the stomach and is then reabsorbed through the 
intestines. Haloperidol or chlorpromazine are rec- 
ommended for continued psychosis. 

See also LSD; Mexican hallucinogenic 

MUSHROOM. 



phenobarbital This barbiturate is used primarily 
to control convulsions as a side effect of poisoning, 
although it has generally been replaced by newer 
anticonvulsant drugs. Because there is a delay in 
onset of the beneficial effects of this drug, other 
anticonvulsants (diazepam or phenytoin) are gen- 
erally tried first. 

phenol Also known as carbolic acid, this is a white 
crystalline substance with a burning taste and a 



phenytoin 187 



distinct acrid odor. It is used in the manufacture of 
fertilizers, paints, paint removers, textiles, drugs, 
and perfumes and is widely used in tlie dye, agri- 
cultural, and tanning industries. In addition, clove 
oil in clove cigarettes contains the phenol derivative 
eugenol and may cause severe breathing problems. 

Phenol is equally deadly whether inhaled, 
absorbed through the skin or eyes or ingested. 
It was once used in households to kill germs but 
has been replaced today by less toxic compounds. 
Hexachlorophene is a chlorinated biphenol that 
was used throughout the United States as a topi- 
cal antiseptic and scrub until its adverse effects on 
the brain were recognized. Other compounds of 
phenol include creosote, creosol, hydroquinone, 
eugenol, dinitrophenol, and pentachlorophenol. 

Poisonous part 

While the mechanism behind its toxicity on the 
central nervous system is not known, phenol can 
cause corrosive injury to the eyes, skin, and respi- 
ratory tract. There are no minimum toxic levels, 
although there have been reports of infants dying 
after repeated skin applications of small doses. 
Adult deaths have occurred after ingestion of 1 to 
32 grams of phenol, although survival after ingest- 
ing 45 to 65 grams has also been reported. There 
have been reports of infant deaths with as small as 
50 to 500 milhgram doses. 

Symptoms 

Phenol is markedly corrosive on any tissue in which 
it comes in contact. Exposure to the eyes can cause 
blindness; contact with the skin (at even low vapor 
concentrations) can cause a delayed burning and 
gangrene, with paleness, weakness, sweating, high 
fever, shock, cyanosis, excitement, frothing, coma, 
kidney damage, and death. Ingesting large amounts 
of phenol can severely burn the mouth and throat 
and can cause abdominal pain, nausea, corrosion of 
the lips, mouth, esophagus, and stomach, cyanosis, 
muscle weakness, collapse, coma, and death. Death 
from phenol poisoning is most likely during hot 
weather when loss of body heat is inhibited. 

Treatment 

Do NOT induce vomiting, because phenol is corro- 
sive and may induce seizures. Ingested poison can 



be treated with milk, olive oil, or vegetable oil fol- 
lowed by repeated gastric lavage. (Neither mineral 
oil nor alcohol should be used, since they speed up 
the absorption of phenol, although some medical 
texts still recommend them.) Castor oil dissolves 
phenols and interferes with absorption. Follow 
with activated charcoal and a cathartic. 

For skin contact, wash the area for 15 minutes 
followed by the application on the skin of castor 
oil, olive oil, or petroleum jelly. For eye contact, 
immediately flush with tepid water or saline. 

See also creosote. 



phentolamine This vasodilator acts rapidly on 
both blood vessels and arteries (within two min- 
utes) and is used to treat high blood pressure 
following overdose of phenylpropanolamine or 
stimulant drugs such as amphetamine, cocaine, or 
ephedrine. 

See also amphetamines; cocaine; deconges- 
tants; EPHEDRINE. 

phenurone See sleeping pills. 

phenylpropanolamine See decongestants. 

phenytoin (Dilantin) This epileptic drug is used to 
prevent seizures and may easily cause an accidental 
overdose in persons in chronic therapy because 
of drug interactions or slight dosage adjustments. 
Poisoning may occur either by an acute overdose 
by mouth or by chronic overmedication. Poison- 
ing may also occur following rapid intravenous 
administration. Persons with kidney problems may 
experience toxicity at lower levels. 

Symptoms 

Mild symptoms include nystagmus (involuntary 
movement of the eyeball), nause, vomiting, agita- 
tion, irritability, and hallucinations. At high levels 
of overdose, symptoms include stupor, coma, and 
respiratory arrest. The toxicity to the heart that 
occurs with rapid intravenous injection does not 
result from oral overdose. 



188 philodendron 



Treatment 

There is no specific antidote. Treat symptoms, 
induce vomiting or perform gastric lavage followed 
by tfie administration of activated cfiarcoal and a 
cathartic orally or by gastric tube. 

philodendron (Philodendron) This is the most 
popular houseplant in the United States, but eating 
the leaves can cause painful swelling and blisters in 
the mouth. This climbing vine has aerial roots and 
large, heart-shaped or notched leaves, sometimes 
with variegated patterns. 

Poisonous part 

The leaves contain raphides of calcium oxalate and 
other, unidentified proteins. The oxalates are insolu- 
ble and therefore do not cause systemic poisoning. 

Symptoms 

Pain and swelling of the lips, mouth, tongue, and 
throat; contact dermatitis is also possible. 

Treatment 

Pain and swelling fade by themselves, but keeping 
cold liquid in the mouth (such as milk) can help. 
See also oxalates. 



philodendron, split leaf (Monstera deliciosa) [Other 
names: breadfruit vine, cut leaf philodendron, fruit 
salad plant, hurricane plant, Mexican breadfruit, 
shingle plant, swiss cheese plant, window plant, 
windowleaf.] This woody climber has thick leaves 
with irregular holes. Grown as an indoor plant in 
the United States and native to Mexico, it is also 
cultivated in the West Indies, Hawaii, and Guam. 

Poisonous part 

The leaves are toxic and contain raphides of cal- 
cium oxalates. 

Symptoms 

After eating, the lips, mouth, and tongue begin to 
burn and swell followed by an acute inflammatory 
reaction. Because eating the leaves of this plant 
is quickly painful, there is little danger that large 
amounts will be ingested. 



Treatment 

The pain and swelling will fade by themselves, 
but cool liquids (such as milk) held in the mouth, 
together with painkillers, may help ease the pain. 
The insoluble oxalates in these plants don't cause 
systemic poisoning. 
See also oxalates. 



phosgene Once manufactured as a weapon for 
chemical warfare, phosgene is now used as an 
industrial gas to manufacture dyes, resins, and pes- 
ticides. In addition, it is often produced during fires 
or while welding metal that has been cleaned with 
chlorinated solvents. 

An irritant, it does not immediately cause symp- 
toms at low doses; for this reason, a person may 
unknowingly inhale the gas over a period of time, 
injuring the lungs. 

Symptoms 

Exposure to mild amounts causes cough and 
some irritation. After 30 minutes to eight hours 
(depending on how long the person was exposed) 
further symptoms develop: labored breathing and 
swelling in the lungs; and permanent lung dam- 
age may result because phosgene is changed in 
the alveoli into hydrochloric acid, causing dam- 
age and inflammation of the small airways and 
tissue. 

Treatment 

There is no specific antidote. Treat symptoms and 
give supplementary oxygen if needed. 

phosphate esters A group of highly toxic com- 
pounds that are used as insecticides and are 
extremely poisonous to humans and animals; they 
are quickly absorbed from the skin, lungs, and gas- 
trointestinal tract. The greatest hazard to humans 
from these insecticides is through breathing the 
compounds, which is three times more toxic than 
oral exposure and 10 times more toxic than skin 
absorption. These esters were discovered acciden- 
tally by the Germans during World War II in their 
search for poison gas. 



physostigmine 189 



Symptoms 

Weakness, unsteadiness, blurred vision, vomiting, 
abdominal cramps, diarrhea, salivation, sweating, 
tremors, and problems in breathing. 

Treatment 

Administration of atropine, supportive therapy as 
required. 

See also insecticides. 



phosphine This colorless gas is heavier than air, 
and, while rarely causing poisoning in the general 
public, it does present a hazard to metal refiners, 
acetylene workers, fire fighters, and pest-control 
operators. Phosphine is a highly toxic gas of partic- 
ular danger to the lungs, brain, kidneys, heart, and 
liver. Chronic exposure to less-than-lethal dosages 
can also produce toxic symptoms. 

Symptoms 

Inhalation causes severe lung irritation, cough, 
labored breathing, headache, dizziness, lethargy, 
and stupor followed by seizures, gastroenteritis, 
and kidney and liver problems. Symptoms usually 
appear fairly soon after inhalation, except in the 
case of chronic low-level exposure. 

Treatment 

There is no specific antidote. Treat symptoms, and 
provide supplemental oxygen if needed. 

phosphorus A chemical used as an inorganic 
insecticide and also in the manufacture of fertil- 
izers and fireworks. As a red, granular insoluble 
substance, phosphorus is nontoxic, but its yellow 
or white form is highly poisonous and ignites on 
contact with moist air and water, trailing white 
fumes and burning with an eerie green light. At 
one time, phosphorus was used on the tips of 
matches, but it has since been replaced because of 
its toxicity. 

Phosphorus is highly corrosive and a general 
cellular poison; the fatal dose of white-yellow 
phosphorus is about one milligram per kilograms, 
although deaths have been reported from ingesting 
as little as 1 5 milligrams. 



Symptoms 

Immediately after ingestion, yellow phosphorus 
begins to affect the digestive tract, causing abdominal 
pain, nausea, vomiting luminescent material, and 
diarrhea. Cardiac collapse may occur because of fluid 
loss from vomiting and diarrhea and because of direct 
toxicity on the heart. It is possible that death may 
occur within 12 hours after ingestion. If not, there 
may follow one to three days with no symptoms, 
during which time phosphorus begins to damage the 
liver and muscle, heart, kidney, and nervous system; 
after about three days the symptoms will return, 
much more serious this time with liver enlargement, 
jaundice, delirium, convulsions, and coma. 

Death may not occur until three weeks following 
ingestion. Phosphide (rat poison) ingestion causes 
jaundice, pulmonary edema, and cyanosis (blue 
skin color) and can be fatal within one week. 

There is also a problem with skin contamina- 
tion: If yellow phosphorus dries on the skin, it can 
cause a second- or third-degree burn. 

If the phosphorus vapor is inhaled, symptoms 
appear within two days and include conjunctivi- 
tis, nausea, vomiting, fatigue, coughing, jaundice, 
tremors, numbness, low blood pressure, pulmonary 
edema, collapse, heart problems, convulsions, and 
coma. Inhalation may be fatal within four days to 
two weeks. The classic sign of chronic poisoning 
is called "phossy jaw," an aching and swelling of 
the jaw followed by deterioration of the jawbone, 
in addition to weakness, weight loss, anemia, and 
spontaneous fractures. 

Treatment 

There is no specific antidote. Eliminate exposure and 
give oxygen. With ingestion, perform gastric lavage 
followed by the administration of activated charcoal 
and a cathartic, although there is no evidence that 
charcoal absorbs phosphorus. Provide symptomatic 
and supportive treatment. Do not induce vomiting. 
For skin contamination, wash with plenty of water. 
For chronic poisoning causing jaw necrosis, surgical 
excision of affected jawbone may be required. 
See also insecticides. 



physostigmine A treatment used in poisoning 
cases with symptoms of agitated delirium, heart 



190 phytonadione 



rhythm disturbances (sinus tachycardia), and high 
fever with no sweating. It is NOT used as an anti- 
dote for cychc antidepressant overdose, nor at the 
same time as certain neuromuscular blockers (such 
as succinylcholine). 

See also parasympathomimetic drugs. 

phytonadione See Vitamin K. 

phytotoxins Also called toxalbumins, these are 
extremely deadly protein molecules (similar to 
bacterial toxins) that are produced by a few plants, 
including the castor bean, rosary pea, and black 
locust. In a manner similar to that of bacterial 
toxins, the phytotoxins elicit an antibody response 
after ingestion. Eating just one seed from a plant 
containing these toxins can be fatal. Most phytotox- 
ins are destroyed by heat. 

Interestingly, however, different people will 
react differently to the presence of phytotoxins. 
Symptoms include gastrointestinal irritation, with 
lesions and swelling of organs. 

See also black locust; castor bean; rosary pea. 

pilocarpine See parasympathomimetic drugs. 

pit vipers Seventeen of the 19 venomous snakes 
in North America belong to this family of dan- 
gerous poison snakes, which includes about 290 
species. There are three genera in the family: Agkis- 
trodon (copperheads and cottonmouths), Crotalus, 
and Sistrurus (both rattlesnakes). 

Pit vipers seem to be extremely highly evolved 
snakes very well designed for capturing, killing, 
and eating fairly large, warm-blooded prey. Most 
have stout bodies with wide heads, patterned with 
crossbands and blotches and with retractable hol- 
low fangs in the front of the upper jaw. The fangs 
can be folded back and then positioned forward as 
the mouth opens to strike. The pit viper's name 
comes from the heat-sensitive pits located on each 
side of the head between the nostril and the eye, 
which is used to locate its prey. 

Seriousness of the bite depends on a wide vari- 
ety of variables, including the snake's size (usually 



the larger, the more venomous) and whether the 
snake is hungry or alert. The angle of the bite and 
its depth and length also affect the seriousness 
of the bite. In addition, the size of the victim can 
be important (children and infants are at greater 
risk), and the health of the victim at the time 
of the bite will also affect the outcome. Persons 
with diabetes, hypertension, or blood coagulation 
problems and the elderly are particularly sensitive 
to snake venom, and menstruating women may 
bleed excessively following the bite of a pit viper. 
Several cases of miscarriage have been reported 
when pregnant women have been bitten. Finally, 
the location of the bite itself is crucal to its serious- 
ness; venomous snake bites on the head and trunk 
are twice as serious as those on the extremities, 
and bites on the arms are more serious than those 
on the legs. 

Poisonous part 

The venom of the pit vipers is a mixture of pro- 
teins that acts on a victim's blood. Even snakes 
that appear to have been killed by the side of the 
road have been reported to bite. The size of the 
snake can give an idea of its potential dangerous- 
ness and can be judged by the distance between 
the fang marks. Fang marks less than 8 millimeters 
apart would be a small snake; between 8 and 12 
millimeters indicates a medium-size snake, and 
more than 12 millimeters suggests a large venom- 
ous snake. Even snakes that have been "defanged" 
can be dangerous, since all snakes grow new fangs 
from time to time. 

Symptoms 

Swelhng, internal bleeding, changes in red blood 
cells, central nervous system symptoms including 
convulsions and sometimes psychotic behavior, 
muscle weakness, and paralysis. In addition, there 
are general systemic symptoms of fever, nausea, 
vomiting, diarrhea, pain, and restlessness. Tachy- 
cardia and bradycardia can develop, and kidney 
failure has been reported. 

Treatment 

Within the first 30 to 45 minutes after the bite of 
a pit viper, apply a venous tourniquet a few inches 
above the bite, loosening it every 15 to 30 min- 



plant safety 191 



utes and reapplying it above the level of progres- 
sive swelling. Keep the victim quiet, lying down 
to decrease metabolic activity (which affects the 
spread of the venom). The wound area (especially 
if it is an arm or leg) should be kept lower than 
the heart. Within 30 minutes, trained individu- 
als can incise the wound area and apply suction. 
Antivenin is available but should be administered 
within four hours; antivenin is rarely helpful if 
given more than 12 hours after the bite. Tetanus 
prophylaxis is advisable; other treatment might 
include blood transfusions, intravenous fluids, 
treatment for convulsions, and antihistamines to 
control itching. In addition, broad-spectrum anti- 
biotics may be administered, since snakebites are 
notorious for becoming infected. If antivenin has 
not been administered (or was given hours after 
the bite), sloughing of the skin around the bite is 
common. 

While certain anecdotal reports in the popular 
press have reported that some individuals become 
immunized after many bites of the pit viper, scien- 
tifically controlled attempts to develop immunity 
in human beings have failed. 

See also copperhead snake; rattlesnake, cane- 
brake; RATTLESNAKE, CASCABEL; RATTLESNAKE, EAST- 
ERN diamondback; rattlesnake, Mexican west 
coast; rattlesnake, red diamondback; rattle- 
snake. South American; rattlesnake, timber; 
rattlesnake, western diamondback; snakes, poi- 
sonous; WATER MOCCASIN. 

plant safety Plants are a potential form of poi- 
soning, especially for very young children who are 
likely to put plants — especially those with berries 
or other brightly colored parts — into their mouths. 
You are probably aware of some of the well-known 
poisonous plants, but did you know that a child 
can become seriously ill from biting into a daffodil 
bulb or drinking the water out of a vase holding 
lilies of the valley? 

Teach your children from the very beginning 
that they should NEVER put a plant into their 
mouth without first checking with an adult. This 
must include ALL mushrooms found in the wild. 

If, despite all of your precautions, your child has 
eaten a plant: 



• Stay calm and check your child for adverse 
reactions. 

• Determine how much of the plant and what 
parts (e.g., berries, flowers, leaves) have been 
eaten. 

• Remove any uneaten plant material from the 
child's mouth; check for redness, blisters, swell- 
ing, irritation, and cuts 

• Observe for allergic reactions: blotchy red skin, 
swelling, breathing problems, nausea, diarrhea 

• Identify the plant: if someone else is in the 
house, send him or her to a nursery to identify 
the plant if you do not know its name 

• Call the poison control center (see Appendix F 
for a list of regional centers). Report any adverse 
reactions and give the age and weight of the 
child. 

• If told to go to a hospital, take the plant or a 
sample with you. 

• If your child is too young to speak, retrace the 
child's steps and check for any damaged plants. If 
there is plant material in the mouth, try to match 
it with a plant in the area. 

Child-safe plants 

If you enjoy having plants and flowers in your 
home but have small children, you can still deco- 
rate with greens. Just choose safe plants that will 
not hurt your children even if they swallow the 
plant. Here is a list of safe plants: 



African violet 


dandelion 


aluminum plant 


Easter lily 


aspidistra 


gardenia 


aster 


impatiens 


baby's tears 


jade plant 


begonia 


kalanchoe 


bird's nest fern 


lipstick plant 


Boston fern 


magnolia 


bougainvillea 


marigold 


California poppy 


nasturtium 


camellia 


Norfolk Island pine 


Christmas cactus 


pepperomia 


coleus 


petunia 


creeping Charlie 


poinsettia 


dahlia 


prayer plant 



192 Plesiomonas shigelloides 



purple passion 
rose 

sensitive plant 
spider plant 
Swedish ivy 
tiger lily 



umbrella tree 
violet 

wandering Jew 
wax plant 
wild strawberry 
zebra plant 



Plesiomonas shigelloides This bacterium is 
found in water, freshwater fish, and shellfish, and 
causes a type of gastroenteritis among people in 
tropical or subtropical areas. Because most infec- 
tions are mild, people don't seek medical treat- 
ment. It is not commonly reported in the United 
States, but this may be becauses cases are included 
as a group of diarrhea diseases of unknown origin 
that respond to broad spectrum antibiotics. Many 
cases that may be reported in the United States 
involve people with preexisting health problems 
or very young patients. A cluster occurred in North 
Carolina in 1980, when 36 out of 150 people at an 
oyster roast experienced symptoms two days later. 
In June 1996, an outbreak occurred following a 
private party attended by 189 people, 30 of whom 
became ill. The offending food — macaroni salad, 
potato salad, and baked ziti — had been catered. 
The cause of the P. shigelloides outbreak was traced 
to contaminated well water used by the catering 
facility. 

Most cases appear to be related to tainted water 
that is drunk or used to rinse vegetables eaten 
raw. 

Symptoms 

Symptoms usually appear within a day or two after 
eating or drinking tainted food or water and include 
fever, chills, abdominal pain, nausea, watery diar- 
rhea, or vomiting. In severe cases, diarrhea may 
be foamy, greenish yellow, or tinged with blood. 
While the diarrhea is mild in most people, infants 
and young children may have high fever and chills; 
blood poisoning and death have occurred among 
those with faulty immune systems, or who are seri- 
ously ill with cancer or blood disorders. 

Treatment 

Most people recover on their own without 
treatment. 



plum cherry pit See Prunus. 



poinsettia (Euphorbia pulcherrima) This popular 
Christmas plant has a long-standing poisonous rep- 
utation, but there are only two cases of fatal poi- 
soning by poinsettia in toxicological literature. All 
references to poinsettia as potentially lethal have 
been traced to one case in 1 91 9 when a Hawaiian 
child was reported to have died after eating poin- 
settia. However, researchers in the 1970s found 
that poinsettia was not lethal; several rat studies 
showed that large amounts of poinsettia could be 
eaten without harm. While some authorities and 
many popular magazines still report poinsettia as 
poisonous, most experts now agree that it is virtu- 
ally certain poinsettia is not. 

In the 1988 annual report of the American 
Association of Poison Control Centers National 
Data Collection System, there were no serious poi- 
sonings reported out of 3,001 exposures during the 
rating period. 

However, it may be possible that the plant's 
milky sap may cause mild abdominal pain with 
vomiting and diarrhea if ingested. Locally, this sap 
can cause skin and mucous membrane irritation. 



poison control centers This network of more 
than 60 poison control centers across the country is 
available free of charge, 24 hours a day with poison 
treatment information. The idea had its roots in a 
report by the American Academy of Pediatrics in 
1952, when an academy survey that year revealed 
that half of all household accidents involving chil- 
dren was due to some type of poisoning. The study 
noted that most of the poisonings were caused by 
common over-the-counter and prescription drugs, 
and cleaning products. Flavored children's aspirin, 
which had then been only recently introduced, was 
responsible for one-fourth of all poisoning cases 
in children under age five, resulting in about 400 
deaths a year. 

This report set off alarm bells at the academy 
and was responsible for the introduction of the first 
"child-proof" caps on aspirin bottles, responsible 
for the almost complete elimination of childhood 
aspirin poisoning cases. 



poisoning, emergency 193 



A year after the academy's accident prevention 
study was completed, the first poison control cen- 
ter was established in Chicago under the leadership 
of the Illinois chapter of the American Academy 
of Pediatrics. A few months later, the Duke Uni- 
versity Poison Control Center was begun in North 
Carolina. 

With the appearance of these two centers, the 
idea of poison control centers spread across the 
country. In 1957, the Food and Drug Administra- 
tion established the National Clearinghouse for 
Poison Control Centers in order to coordinate 
activities at poison control centers across the 
United States. The clearinghouse collected and 
standardized product toxicology data, reproduced 
this information on large file cards and distributed 
them nationwide to poison control centers. 

At about the same time, the American Academy 
of Pediatrics and the American Pediatric Health 
Association established the American Association 
of Poison Control Centers. See Appendix F for a list 
of regional poison control centers. 

poisoning, emergency You may never need to 
handle a poisoning emergency, but you should be 
prepared for the possibility. Here are the guidelines: 

• Post the number of your nearest poison control 
center on your phone. The number should be 
listed on the inside front cover of your local tele- 
phone directory. Regional numbers are listed in 
Appendix F of this volume. 

• If you suspect or know that poisoning has 
occurred, call your nearest poison control center 
immediately. If you have not placed the num- 
ber by the phone or cannot find it, call 911, the 
operator, or your local emergency number. 

• When you reach someone at the poison control 
center or a doctor, be prepared to offer the fol- 
lowing information: 

• Your name 

• Victim's name, age, and weight 

• Name or kind of poison (name on bottle, 
ingredients, type of plant, etc. ) 

• How much of the poison was consumed 



• When the poison was consumed 

• Symptoms 

• Other medical problems the victim may have, 
such as diabetes, heart problems, asthma, epi- 
lepsy, or high blood pressure 

• Any drugs (including over-the-counter) that 
the victim may take regularly 

• Whether the victim has vomited 

• Whether you have given the victim anything 
to eat or drink 

The personnel at the poison control center will 
tell you whether or not to induce vomiting. Some 
poisons, such as acids or alkalies, should not be 
brought up. If you do not know the identity of the 
substance that was swallowed, DO NOT induce 
vomiting. 

Poison control may recommend that you use 
activated charcoal, Epsom salts, or specific products 
to neutralize the poison. Always follow the instruc- 
tions given by a poison control center. DO NOT 
trust antidote information given on product labels, 
and do not use mustard or salt to induce vomiting. 
These old-fashioned methods do not work well. 
First aid procedures differ according to the kind 
of poison involved and how it entered the body, 
the victim's weight, how long the poison has been 
working, and other factors. Only expert medical 
personnel can determine the correct procedures. If 
you try to treat the victim yourself without expert 
advice, you may do further harm. 

Other tips to remember when there is a poison- 
ing emergency: 

• Do not give a saltwater solution, especially to 
children. Use of saltwater was a recommenda- 
tion from the past, but it can be potentially dan- 
gerous and if given repeatedly it can cause salt 
intoxication, seizures, and death. 

• Do not administer fruit juice or vinegar to neu- 
tralize an alkali. Studies show that if you give an 
acid to neutralize a base it produces heat, which 
increases the possibility of a burn injury. 

• Do not use sodium bicarbonate, chalk, or soap 
to treat an acid poisoning. Studies suggest that 
giving a base to neutrahze an acid can release 



194 poisonings, in home 



carbon dioxide gas, stretch the stomach, and 
even cause it to rupture. 

• Do not give milk to coat the digestive tract. Milk 
may bind syrup of ipecac and interfere with 
vomiting. If the victim consumed a petroleum 
substance, milk may cause vomiting, which 
could introduce the substance into the lungs. 

• Dilution with water or milk should be done 
only when a corrosive poison has been swal- 
lowed. For other types of poison, milk or water 
will actually increase the rate of absorption by 
causing the substances to dissolve more rapidly. 
A stomach filled with water or milk will force 
its contents through the sphincter between the 
stomach and the small intestines, where they 
will be absorbed faster. However, water can be 
given when using ipecac syrup. 

poisonings, in home You may think of your home 
as an oasis of safety in an unsafe world, and for the 
most part that may be true. But your home can be a 
very dangerous place for youngsters when it comes 
to accidental poisoning, where even one tablet of 
certain medications can kill a young child. 

More than 2.4 million cases of poisoning are 
reported to poison centers across the United States 
each year. Among those, most accidental poison- 
ings occur among children under the age of six 
because this age group is especially curious about 
everything in their environment, and their bodies 
are small enough so that a relatively small amount 
of a toxin can be fatal. 

Common poisons 

The substances most often consumed by children 
under age five, according to the Poison Control 
Centers, are: 

Plants 

Soaps, detergents, cleaners 
Perfume, cologne, toilet water 
Antihistamines, cold medications 
Vitamins, minerals 
Aspirin 

Household disinfectants, deodorizers 
Insecticides 

Miscellaneous painkillers 



Fingernail preparations 
Liniments 
Household bleach 
Miscellaneous external medicines 
Cosmetic lotions, creams 

Other common, potentially dangerous products 
found in nearly every home and garage include 
polishes and waxes, alcohol, hair dyes, garden 
products (roach powders, rat pellets, weed kill- 
ers, lime, sprays), and garage products (antifreeze, 
kerosene, gasoline, pain thinners, and strippers). 

Prevention 

Parents should make a rule that all hazardous items 
be kept in high cupboards, on tall shelves in closets 
or in locked drawers or cabinets. All toxic products 
should be returned to their secure cabinets after 
every use. 

• In the kitchen, keep all household chemical 
products out of sight and locked up when they 
are not being used. Do not keep chemicals stored 
under the sink and on the counters because they 
are within easy reach of most youngsters. 

• Make sure all harmful products have child- 
resistant caps. 

• Keep all harmful products in their original con- 
tainers. Original labels often give first aid infor- 
mation in the event of poisoning, and products 
stored in other containers may look like food to 
a child. 

• Keep harmful products stored in a place separate 
from food. 

• In the garage and utility rooms, keep the fol- 
lowing items in a locked cabinet with childproof 
latches: antifreeze, windshield washing fluid, 
gasoline, kerosene, and other automobile fluids; 
also pesticides and other garden products (see 
"Pesticide Safety"). 

poison ivy (Toxicodendron radicans) Poison ivy 
is one of the most common plants in the United 
States that are poisonous to touch; it causes a 
contact dermatitis in most people — as many as 87 
million Americans. 



poison ivy 195 



The leaves of the poison ivy plant are glossy 
green, may be notched or smooth and almost 
always grow in groups of three — two leaves oppo- 
site each other and one at the end of the stalk. 
However, according to some experts there are 
exceptions, and leaves may sometimes appear in 
fives, sevens, or even nines. In early fall, the leaves 
may turn bright red. Although it usually grows as 
a long, hairy vine — often wrapping itself around 
trees — it can also be found as a low shrub growing 
along fences or stone walls. Poison ivy has waxy 
yellow-green flowers and greenish berries that look 
rather like a peeled orange. These berries can help 
in identification of the plants in late fall, winter, 
and early spring before the leaves appear. 

Poison ivy is found throughout the United 
States, but it is most common in the eastern and 
central states. 

Poisonous part 

Poison ivy, poison oak, and poison sumac are 
closely related species, all three containing a 
colorless or slightly yellow resin called urushiol, 
which comes from a Japanese word meaning "lac- 
quer." Skin contact with urushiol causes an aller- 
gic reaction known as contact dermatitis in many 
individuals. While each of these three plants 
contains a slightly different type of urushiol, they 
are so similar that individuals sensitive to one will 
react to all three. The entire plant contains uru- 
shiol and is therefore poisonous: leaves, berries, 
stalk, and roots. 

Urushiol is easily transferred from an object 
to a person, so anything that touches poison 
ivy — clothing, gardening tools, a pet's fur, athletic 
equipment, sleeping bags — can be contaminated 
with urushiol and cause poison ivy in anyone who 
then touches the object. Urushiol remains active 
for up to one year, so any equipment that touches 
poison ivy must be washed. Even the smoke from 
burning poison ivy is toxic and can irritate the skin 
of the face, eyes and lungs, since urushiol can be 
carried in smoke. It can irritate the throat if eaten. 
Individuals should never burn poison ivy plants as 
a way to get rid of them, since the smoke given off 
by these burning plants is particularly dangerous 
and can enter the nasal passages, throat, and lungs 
of anyone who breathes it. 



As the leaves die in the fall, the plant draws 
certain nutrients and substances (including the 
oil) into the stem. But the oil remains active, so 
that even in winter it may cause rash if the broken 
stems are used as firewood kindling or vines on a 
Christmas wreath. 

Symptoms 

While not every person is allergic to poison ivy, 
about seven out of 10 Americans are sensitive 
to urushiol and will develop contact dermatitis if 
exposed to a large enough dose. 

Symptoms vary from one person to the next; 
some people exhibit only mild itching, while oth- 
ers experience severe reactions, including severe 
burning and itching with watery blisters. The 
skin irritation, swelling, blisters, and itching may 
appear within hours or days, usually develop- 
ing within 24 to 48 hours in a sensitized person. 
The skin becomes reddened followed by watery 
bhsters, peaking about five days after contamina- 
tion and gradually improving over a week or two, 
even without treatment. Eventually, the blisters 
break, and the oozing sores crust over and then 
disappear. 

About 15 percent of the people who are allergic 
to poison ivy, poison oak, and poison sumac are so 
highly sensitive that they react within four to 12 
hours instead of 24 to 48. These individuals often 
experience swollen eyes, rapidly developing blis- 
ters that ooze pus, and fever. 

Despite common misconception, poison ivy is 
not spread by scratching open blisters or skin-to- 
skin contact but by the oil (urushiol) found in 
the plant. Anything that brushes against this oil 
is contaminated and can pass on poison ivy if it 
brushes the skin. Poison ivy is not spread from 
person to person, by touching bhsters, since only 
the oil spreads the rash. For this reason, doctors 
recommend not scratching bhsters because any 
remaining urushiol that hasn't been washed off can 
be transmitted to another part of the body. In addi- 
tion, scratching blisters may cause infection from 
germs on the fingernails. Animals can also transmit 
poison ivy from their fur to their owners' skin. Any 
animal suspected of coming in contact with poison 
ivy should be given a bath; wear protective gloves 
when bathing affected animals. 



196 poison oak 



In addition, allergy to poison ivy, oak, and 
sumac may also mean a person is allergic to related 
plants, including cashews, pistachios, mangos, and 
Chinese or Japanese lacquer trees. 

Treatment 

The best treatment is to wash the affected area 
immediately after contact (within 10 minutes, if 
possible) with yellow laundry soap and cold water, 
or water from a shower. Do not bathe in a tub, 
as this could spread the oil. Do not scrub with 
a brush. If contaminated while in isolated areas, 
wash in a cold running stream. Any clothing that 
might have come in contact with urushiol must 
be washed several times. If the urushiol is washed 
off, there is little further treatment needed of mild 
cases of the rash. Remove rings, watches, brace- 
lets, etc., before washing hands. Wash contami- 
nated jewelry. 

Early application of topical steroids minimizes 
the severity of dermatitis; systemic steroids given 
during the first six hours after exposure are the 
most effective. 

Itching can be treated with compresses soaked 
in cold water. A calamine lotion spread over the 
rash will help relieve the itching and burning and 
dry the area. Products containing local anesthetics 
(such as benzocaine) or irritants (camphor or phe- 
nol) should be avoided. Systemic antihistamines do 
not work against the rash, although their sedative 
action may help the person sleep. In the case of a 
severe reaction, a physician may prescribe cortico- 
steroid drugs by mouth or injection. 

Prevention 

New barrier creams (bentoquatam) may offer some 
protection; these have been recently approved by 
the U.S. Food and Drug Administration. Cream 
should be applied 15 minutes before exposure and 
every four hours afterward. It should not be used 
if a rash is already present, nor by children under 
age six. Dermatologists are also working on a skin 
treatment to prevent the oil from penetrating the 
skin. 

Most people could be immunized against poi- 
son ivy through prescription pills, which contain 
gradually increasing amounts of active extract 
from the plants. However, this procedure can take 



four months to achieve a reasonable degree of 
"hyposensitization," and the medication must be 
continued over a long period of time. In addition, it 
often causes uncomfortable side effects such as skin 
problems, stomach problems, fever, and inflamma- 
tion. Convulsions have occurred in children fol- 
lowing oral doses of the plant's extract. 

This procedure is recommended only if the doses 
are given before contact with the plant, and only 
for people (such as firefighters) who must live or 
work in areas where they come into constant con- 
tact with poison ivy. Consult your dermatologist 
for his or her advice on whether you should con- 
sider this type of immunization. Allergy shots also 
are available to help prevent recurring episodes of 
poison ivy, poison oak, and poison sumac. Because 
these shots are often ineffective, however, they 
should be used only by people who are extremely 
sensitive to urushiol. 

See also poison oak; poison sumac; urushiol. 

poison oak (Toxicodendron diversilobum) A plant 
poisonous by touch, this is one of three closely 
related species containing similar forms of the resin 
urushiol. Urushiol causes a contact dermatitis in 
seven out of 10 Americans who come in contact 
with it. The leaves of poison oak occur in groups 
of three and are very similar to oak leaves, from 
which the plant gets its name. The underside of the 
leaves are much lighter green than the tops because 
of the thousands of tiny fine hairs that cover them. 
Berries may be greenish or creamy white, although 
not all plants bear fruit. Poison oak usually grows 
as a low shrub on the west coast from Mexico to 
British Columbia. 

Symptoms 

Symptoms vary from one person to the next, rang- 
ing from mild itching to severe burning and itching 
with watery bhsters, and usually develop within 
24 to 48 hours in a sensitive person. Symptoms 
usually peak about five days after contamination 
and gradually improve over a week or two even 
without treatment. Eventually, the bhsters break, 
and the oozing sores crust over and then disappear. 
Poison oak is not spread by scratching open blisters 
but by the urushiol found in the plant. Anything 



poisons, by symptom 197 



that brushes against this oil is contaminated and 
can pass on poison oak if it brushes the skin. For 
this reason, doctors recommend not scratching 
blisters, since any remaining urushiol that hasn't 
been washed off can be transmitted to another part 
of the body. Animals can also transmit poison oak 
from their fur to their owners' skin. Any animal 
suspected of coming in contact with poison oak 
should be given a bath (gloves should be worn). 

Treatment 

The best treatment is to wash the affected area 
immediately after contact with yellow laundry 
soap and cold water, lathering several times and 
rinsing the area in running water after each suds- 
ing. Do not scrub with a brush. If contaminated 
while in isolated areas, wash in a cold running 
stream. Any clothing that might have come in con- 
tact with urushiol must be washed several times. 
If the urushiol is washed off the skin, there is little 
further treatment needed in mild cases. Itching can 
be treated with compresses soaked in cold water, 
and calamine lotion spread over the rash will help 
relieve the itching and burning. In the case of a 
severe reaction, a physician may prescribe cortico- 
steroid drugs by mouth or injection. 
See also poison ivy; urushiol. 



poisons, by symptom Sometimes it is not so easy 
to figure out exactly what poisonous substance 
someone has ingested — especially if the person is a 
young child. If all you have to go on is a symptom, 
it can help to have a way to link symptoms to poi- 
sonous substances. 

Remember that most poisons cause more than 
one symptom, and that the severity of the symp- 
toms differs depending on how much of the poison 
was ingested. 

Aggression 

atropine, belladonna, ketamine, PCP, Preludin 
Anxiety 

amphetamines, barium, bronchial tube relaxers, 
camphor, carbon monoxide, ecstasy, mercury, 
Minipress, PCP, potassium, sodium fluoroacetate, 
Thyrolar, water hemlock, yellow jessamine 



Blood problems 

Many poisons can cause a variety of blood-related 
symptoms, including anemia, hemorrhages (exces- 
sive bleeding), high or low blood sugar, or a low 
red blood count. 

Anemia Dilantin, pathalene, rattlesnake, 
trinitrotoluene 

Bleeding aspirin, atophan, Depakene, 
warfarin 

Blood Sugar — High Lasix, Vacor 

Blood Sugar — Low akee, Amanita mush- 
room, Dilantin, Inderal, insulin, phosphorus 

Hemorrhage adder, aspirin, atophan, castor 
bean, chlordane, cinchona bark, cottonmouth, 
Depakene, fer-de-lance, isopropanol, paternoster 
pea, potassium permanganate, rhubarb, savin, 
Vacor, warfarin 

Low Red Blood Count carbon monoxide, 
ethinamate, warfarin 

Bruises 

See SKIN problems. 

Collapse 

A variety of poisonous substances are serious 
enough that, when ingested, they can trigger a 
total collapse. The following poisons may cause 
collapse: 

adder, ammonia, bromates, cantharidin, castor 
bean, cationic detergents, chloramine-T, cinchona 
bark, cottonmouth, ethylene chlorohydrin, form- 
aldehyde, Haldol, Indian tobacco, ipecac, lead, 
narcissus, nicotine, nitroglycerin, privet, procaine, 
silver nitrate, stingray, Vacor 

Coma 

akee, aldrin, amphetamines, aniline, antimony, 
arsenic, aspirin, atropine, barbiturates, belladonna, 
boric acid, bromates, bryony, cantharidin, cassava, 
castor bean, Catapres, celandine, chloral hydrate, 
cinchona bark, cinchophen, cocaine, codeine, col- 
umbine, corn cockle, Cortinarius mushroom, croton 
oil, daphne, death camas, dieldrin, Elavil, epineph- 
rine, ergot, ethyl alcohol, GHB, Gyromitra mush- 
room, Haldol, heroin, hydrogen sulfide, Inderal, 
Indian tobacco, insulin, isopropanol, jimsonweed, 
lead, lithium, Lomotil, LSD, mandrake, marijuana, 
morphine, nicotine, nitroglycerin, opium, panther 



198 poisons, by symptom 



mushroom, paral, paternoster pea, PCP, Percodan, 
Permitil, petroleum distillates, phenol, potato, pro- 
caine, rhododendron, savin, selective serotonin 
reuptake inhibitors, silver nitrate, Sinequan, sodium 
fluoroacetate, Stelazine, tetrachloroethane, Thora- 
zine, toxaphene, Vacor, Valium, valproic acid, yew 

Confusion 

amphetamines, aniline, atropine, barbiturates, 
carbon monoxide, carbon tetrachloride, chloral 
hydrate, DDT, Dilantin, endrin, flunitrazepam, 
Inderal, lithium, nicotine, opium, Preludin, selec- 
tive serotonin reuptake inhibitors, sodium thiocya- 
nate, Tagamet, Tylenol 

Convulsions or Seizures 

akee, aldrin, amphetamines, aniline, arsenic, aspi- 
rin, atropine, barium, belladonna, benzene, ben- 
zene hexachloride, benzylpiperazine, betel nut seed, 
boric acid, boron, bromates, bronchial tube relax- 
ers, bryony, caffeine, calcium, camphor, cassava, 
castor bean, cationic detergents, cinchophen, cobra, 
cocaine, columbine, Cortinarius mushroom, cyanide, 
daffodil, daphne, DDT, dieldrin, dyphylline, Elavil, 
elderberry, endrin, epinephrine, ethyl alcohol, fool's 
parsley, gelsemium, grounsel, Gyromitra mushroom, 
hydrangea, Inderal, Indian tobacco, ipecac, jimson- 
weed, ketamine, oleander, Lomotil, LSD, meadow 
saffron, monkshood, monoamine oxidase (MAO) 
inhibitors, moonseed, mountain laurel, narcissus, 
nicotine, panther mushroom, parathion, paternos- 
ter pea, PCP, Permitil, persistent organic pollutants, 
Phenergan, physostigmine, pokeweed, potato, pro- 
cainamide, procaine, pyrethrum, quaalude, Ritalin, 
rhododendron, rotenone, scorpion fish, scorpi- 
ons, selective serotonin reuptake inhibitors, silver 
nitrate, sodium fluoroacetate, sodium thiocyanate, 
spindle tree, Stelazine, stingray, stonefish, strych- 
nine, tansy, TEPP, Thorazine, toxaphene, turpen- 
tine, water hemlock, yellow jessamine, yew 

Delirium 

atropine, benzene, brown recluse spider, cincho- 
phen, corn cockle, ethylene chlorohydrin, fox- 
glove, henbane, horse chestnut, Inderal, iodine, 
jimsonweed, ketamine, lead, meadow saffron, pan- 
ther mushroom, Tagamet, tetrachlorethane, Vacor, 
white snakeroot 



Depression 

amphetamines, ecstasy, ketamine, mountain 
laurel 

Dizziness or Vertigo 

A wide range of poisonous substances can lead to 
either dizziness or vertigo (a sensation in which the 
person feels he or his surroundings are constantly 
spinning or moving). 

Aldomet, aldrin, amphetamines, aniline, arse- 
nic, aspirin, baneberry, Barbados nut, barbitu- 
rates, benzene, bloodroot, bronchial tube relaxers, 
camphor, carbon tetrachloride, chloral hydrate, 
codeine, Cortinarius mushroom, daffodil, dieldrin, 
Dilantin, elderberry, ethylene chlorohydrin, fly 
agaric, gelsemium, geography cone, Gila monster, 
hydrogen sulfide, jimsonweed, Lasix, methanol, 
monkshood, morphine, nicotine, nitroglycerin, 
Norflex, panther mushroom, Percodan, Persantine, 
petroleum distillates, Phenergan, phenol, Preludin, 
procaine, propane, quinidine, Sinequan, sodium 
fluoroacetate, stingray, Tagamet, Thorazine, toxa- 
phene, trichloroethane, turpentine, Vacor, Valium 

Euphoria/Excitemen t 

amphetamines, benzene, Halcion, heroin, LSD, 
marijuana, nitrous oxide, opium, Preludin 

Hair Loss 

A few substances, including arsenic or boric acid, 
may lead to hair loss (alopecia). Medications that 
cause this symptom include Depakene (valproic 
acid), a central nervous system antidepressant, or 
the high blood pressure medicine Minipress (pra- 
zosin hydrochloride). Polonium-210 can also cause 
hair loss. 

Hallucinations 

amphetamines, atropine, belladonna, betel nut 
seed, bronchial tube relaxers, cocaine, Elavil, ethyl 
alcohol, GHB, Haldol, Inderal, lily of the valley, 
LSD, marijuana, mercury, PCP, Preludin, selective 
serotonin reuptake inhibitors, toxaphene, Valium 

Headache 

Aldomet, aldrin, aniline, arsenic, barbiturates. 
Bacillus anthracis, benzene, boron, bronchial tube 
relaxers, cadmium, camphor, carbon monoxide. 



poisons, by symptom 199 



corn cockle, DDT, dieldrin, dyphylline, elderberry, 
ergot, ethylene chlorohydrin, foxglove, galerina 
mushrooms, GHB, hydrogen sulfide, Inderal, jim- 
sonweed, Lasix, lily of the valley, malathion, 
methyl alcohol, Minipress, naphthalene, nicotine, 
nitroglycerin, nitrous oxide, panther mushroom, 
parathion, persantine, persistent organic pollut- 
ants, potato, Preludin, quinidine, stibine, Tagamet, 
TEPP, tetrachloroethane, Thyrolar, trichloroethane, 
tularemia, yellow jessamine 

Hearing Problems 
Deafness/Hearing Loss aspirin, bromates, 
quinine 

Tinnitus aspirin, cinchona bark, Elavil, endrin, 
Gila monster, nicotine 

Heart Problems 

Many poisons act directly on the heart and are 
capable of causing a range of adverse effects. 

Cardiac Arrest bloodroot, calcium, Catapres, 
cocaine, Elavil, ergot, insulin, oleander, Percodan, 
potassium, sodium, Stelazine, Vahum 

Chest Pain beryllium, cadmium, carbon 
monoxide, ergot, foxglove, jellyfish, monkshood, 
Portuguese man-of-war, sea anemone, TEPP, tur- 
pentine, Vacor 

High Blood Pressure amphetamines, bron- 
chial tube dilators, cadmium, Demerol, ecstasy, 
ketamine, monoamine oxidase (MAO) inhibitors, 
PGP, Preludin, scorpion, Sinequan, Thyrolar, yel- 
low jessamine 

Irregular Heartbeat Bacillus anthracis 
(anthrax), barbiturates, benzylpiperazine, black 
hellebore, bloodroot, caffeine, Dilantin, Elavil, epi- 
nephrine, ether, formaldehyde, foxglove, Inocybe 
mushroom, ipecac, nitrous oxide, phosphorus, Por- 
tuguese man-of-war, sodium fluoroacetate, sting- 
ray, Tylenol, valproic acid 

Low Blood Pressure acid, alkalies, aniline, 
arsenic, barbiturates, boric acid, bromates, can- 
tharidin, carbon tetrachloride, Catapres, chloral 
hydrate, cobra, curare, cyanide, dyphylline, Elavil, 
ethylene chlorohydrin, false hellebore, flunitraz- 
epam, fly agaric, Haldol, heroin, Inderal, insulin, 
ipecac, Lasix, monkshood, monoamine oxidase 
(MAO) inhibitors, nitroglycerin, opium, panther 
mushroom, Percodan, Permitil, Phenergan, phy- 



sostigmine, procainamide, procaine, quinidine, 
rhododendron, scorpions, sodium azide, sodium 
thiocyanate, Stelazine, stingray, Tagamet, TEPP, 
Thorazine, trichloroethane, Tylenol, Vacor 

Rapid Heartbeat acid, amphetamines, atro- 
pine, baneberry, belladonna, bromates, caffeine, 
camphor, cocaine, Cortinarius mushroom, croton 
oil, cyanide, digitoxin, dyphylline, ecstasy, elder- 
berry, epinephrine, fool's parsley, foxglove, Hal- 
cion, Haldol, hemlock, insulin, ipecac, marijuana, 
Minipress, monoamine oxidase (MAO) inhibitors, 
morphine, nicotine, paral, paraquat, paternos- 
ter pea, Phenergan, selective serotonin reuptake 
inhibitors, Sinequan, tansy, Thorazine, turpentine 

Slow Heartbeat/Pulse black locust, blood- 
root, carbon tetrachloride, Catapres, codeine, curare, 
dog mercury, false hellebore, fly agaric, foxglove, 
Inderal, larkspur, lily of the valley, monkshood, 
morphine, panther mushroom, physostigmine, rho- 
dodendron, yellow jessamine 

Weak, Irregular Pulse black locust, hemlock, 
Inocybe mushroom, monkshood, valproic acid 

Hyperactivity 

cocaine, cottonmouth, PGP, Preludin, Thyrolar 

Insomnia 

amphetamines, bronchial tube relaxers, caffeine, 
dyphylline, Elavil, endrin, Inderal, Phenergan, Pre- 
ludin, Reglan 

Irritability 

barbiturates, carbon monoxide, cottonmouth, diel- 
drin, lily of the valley, propane 

Itching 

See SKIN PROBLEMS. 

Kidney /Liver Damage 

It's the job of your liver and kidneys to help filter 
poisons from the body; some substances may cause 
kidney damage or complete organ failure. 

Liver Damage arsenic, botulism, Catapres, 
chlordane, Depakene, Dilantin, formaldehyde, 
methanol, monoamine oxidase (MAO) inhibitors, 
potassium permanganate 

Kidney Damage botulism, daphne, Dilan- 
tin, galerina mushrooms, methanol, naphthalene. 



200 poisons, by symptom 



phenol, potassium permanganate, privet, rhubarb, 
tansy, Tylenol 

Kidney Failure cadmium, colocynth, ecstasy, 
excessive fluid intake, mercury, mountain laurel, 
PCP, sodium, turpentine 

Lung Problems 

In overdose or inappropriate dosage, many medi- 
cines and poisons can affect the lungs, causing 
swelling, coughing and breathing problems, and 
even leading to respiratory failure. 

Breathing Problems aldrin, anaphylaxis, 
aniline, antimony, atropine. Bacillus anthrads 
(anthrax), Barbados nut, barbiturates, barium, bel- 
ladonna, benzene, beryllium, betel nut seed, blood- 
root, bronchial tube relaxers, cadmium, calcium, 
camphor, carbon monoxide, carbon tetrachloride, 
cassava, Catapres, chloral hydrate, cobra, cocaine, 
codeine, curare, death camas, dimethyl sulfate, 
Elavil, elderberry, ergot, fer-de-lance, gelsemium, 
geography cone, Gila monster, hemlock, heroin, 
horse chestnut, Inderal, insulin, ipecac, isopropa- 
nol, jellyfish, larkspur, Lasix, Lomotil, malathion, 
meadow saffron, mercury, Minipress, morphine, 
mountain laurel, nicotine, opium, paral, parathion, 
PCP, percodan, petroleum distillates, Phenergan, 
phosgene, pokeweed, potassium, pufferfish, physo- 
stigmine, rattlesnake, rhubarb, scorpion, shellfish 
poisoning, sodium, sodium fluoroacetate, stibine, 
TEPP trichloroethane, turpentine, Vafium, valproic 
acid, water hemlock, yellow jessamine 

Bronchitis dimethyl sulfate, lead dust, mala- 
thion, mold 

Cough acid, ammonia. Bacillus anthrads 
(anthrax), cadmium, hydrogen sulfide, mercury, 
mold, paral, petroleum distillates, potassium per- 
manganate, trinitrotoluene, tularemia, turpentine 

Coughing Blood aspirin, castor bean, 
warfarin 

Pulmonary Edema ammonia, aspirin, anti- 
mony, bronchial tube relaxers, cadmium, epineph- 
rine, formaldehyde, hydrogen sulfide, isopropanol, 
malathion, methanol, parathion, petroleum distil- 
lates, phosgene, quaalude, scorpion, sodium fluor- 
acetate, turpentine 

Respiratory Failure anectine, blue-ringed 
octopus, bryony, cantharidin, cinchona bark, corn 
cockle, ether, fool's parsley, geography cone, Gila 



monster, heroin, meadow saffron, monkshood, 
nicotine, nitroglycerin, oleander, opium, Pavulon, 
procaine, star of Bethlehem, strychnine, Thorazine, 
toxaphene, tubarine, Vacor, water hemlock 

Mouth Problems 

Some plants and other substances can cause symp- 
toms by direct contact with the mouth. 

Drooling cadmium, columbine, death camas, 
fly agaric, Haldol, Inocybe mushroom, lily of the val- 
ley, malathion, mercury, mountain laurel, panther 
mushroom, PCP, Phenergan, rhododendron, silver 
nitrate 

Foaming acid, ammonia, chloramine-T, phe- 
nol, tansy, water hemlock 

Gum Problems adder, cobra, Dilantin, fer-de- 
lance, lead, mercury, polonium-210 

Swelling black hellebore, dimethyl sulfate, 
Inocybe mushroom, potassium permanganate 

Muscle Problems 

Weak or stiff muscles, spasms, or cramps may all be 
caused by some poisons. 

Cramps (leg) Barbados nut, potassium 

Flaccidity calcium, chloral hydrate, mari- 
juana, potassium, Percodan, Valium 

Rigidity ammonia, black widow spider, cam- 
phor, gelsemium, Haldol, ketamine, PCP 

Spasms aldrin, amphetamines, benzene, 
boric acid, caffeine, camphor, cocaine, DDT, diel- 
drin, Dilantin, Elavil, epinephrine, Lasix, lithium, 
LSD, mercury, nicotine, parathion, physostigmine, 
pokeweed, Preludin, procaine, pyrethrum, Reglan, 
rotenone, scorpion, sodium fluoroacetate, sodium 
thiocyanate, strychnine, tansy, TEPP, Thora- 
zine, Thyrolar, Vacor, white snakeroot, yellow 
jessamine 

Stiffness atropine, black widow spider, mari- 
juana, Permitil, strychnine 

Weakness acid, Aldomet, aldrin, barium, 
beaked sea snake, benzene, beryllium, blood- 
root, cadmium, corn cockle, Cortinarius mushroom, 
daphne, death camas, dieldrin, endrin, false hel- 
lebore, gelsemium, Gila monster, hemlock, Indian 
tobacco, Lasix, lead, meadow saffron, Minipress, 
morphine, Norflex, parathion, Persantine, petro- 
leum distillates, potassium, phenol, pokeweed, 
rhubarb, sodium thiocyanate, stibine, stingray. 



poisons, by symptom 201 



Thyrolar, tularemia, Vacor, Valium, white snake- 
root, yellow jessamine, yew 

Paralysis 

Some poisonous substances act on the central ner- 
vous system, causing paralysis. These include: 
atropine, benzene, blue-ringed octopus, botulism, 
bryony, calcium, cobra, croton oil, curare, gelse- 
mium, geography cone, hemlock, jimsonweed, 
monkshood, mountain laurel, narcissus, parathion, 
Pavulon, potassium, pufferfish, pyrethrum, rattle- 
snake, rhododendron, scorpion fish, sea anemone, 
sodium, stonefish, TEPP 

Psychosis 

atropine, camphor, cocaine, Depakene, Dilantin, 
epinephrine, ergot, ethyl alcohol, Halcion, Haldol, 
LSD, marijuana, mercury, Preludin 

Restlessness 

amphetamines, aspirin, black widow spider, heroin, 
horse chestnut, LSD, Preludin, selective serotonin 
reuptake inhibitors, water hemlock 

Shock 

ammonia, baneberry, cadmium, fer-de-lance, 
insulin, iodine, Lasix, malathion, moonseed, phe- 
nol, Portuguese man-of-war, potassium perman- 
ganate, rattlesnake, sea anemone, silver nitrate, 
stingray, yew 

Skin Problems 

Bleeding adder, black widow spider, brown 
recluse spider, cobra, rattlesnake 

Bruises aspirin, Depakene, Lasix, polonium- 
210, warfarin 

Discoloration — Black silver nitrate 

Discoloration — Blue (cyanosis) acid, Ama- 
nita mushroom, amphetamines, anihne, aspirin, 
boric acid, brown recluse spider, castor bean, 
chloral hydrate, chloramine-T, curare, cyanide, 
dimethyl sulfate, epinephrine, ether, ethinamate, 
Gila monster, heroin, hydrangea, Inocybe mush- 
room, jellyfish, larkspur, nitroglycerin, paral, 
paraquat, phenol, phosgene, procaine, TEPP, tetra- 
chloroethane, trinitrotoluene 

Discoloration — Brown acid, potassium 
permanganate 



Discoloration — Red ammonia, atropine, bel- 
ladonna, bronchial tube relaxers, brown recluse 
spider, cyanide, Inocybe mushroom, insulin, lily 
of the valley, nitroglycerin, persantine, procaine, 
pufferfish, turpentine 

Discoloration — Yellow Indian tobacco, nico- 
tine, trinitrotoluene 

Irritation acid, Aldomet, antimony, arsenic, 
atropine, belladonna, benzene hexachloride, boric 
acid, brown recluse spider, cadmium, cantharidin, 
Catapres, croton oil, DDT, dog mercury, ethylene chlo- 
rohydrin, formaldehyde, hydrogen sulfide, larkspur, 
Librax, malathion, Minipress, narcissus, paraquat, 
parathion, phosphorus, pyrethrum, sodium azide, 
Tagamet, tansy, tetrachloroethane, trinitrotoluene 

Itching larkspur, opium 

Necrotic Tissue acid, alkalies, aniline, ben- 
zene, brown recluse spider, cantharidin, cobra, 
cottonmouth, ergot, ether-chloroform, iodine, jel- 
lyfish, mercury, phenol, phosphorus, potassium 
permanganate, rattlesnake, sea anemone, Tylenol 

Paleness malathion, phenol, trinitrotoluene, 
yew 

Swelling adder, anaphylaxis, blue-ringed 
octopus, brown recluse spider, cobra, jellyfish, 
rattlesnake, scorpion fish 

Speech Problems 

blue-ringed octopus, chloral hydrate, codeine, 
curare, ethyl alcohol, gelsemium, GHB, Haldol, 
ketamine, lithium, marijuana, pufferfish, Thora- 
zine, yellow jessamine 

Stomach or Intestinal Problems 
Abdominal Pain alkalies, Amanita mush- 
room, ammonia, arsenic, aspirin, baneberry, bar- 
ium, bloodroot, bromates, cantharidin, carbon 
tetrachloride, cassava, cinchophen, cocaine, colo- 
cynth, corn cockle, daffodil, daphne, fool's pars- 
ley, formaldehyde, hydrangea, iodine, isopropanol, 
jellyfish, lead, lily of the valley, meadow saf- 
fron, mercury, methanol, Minipress, mountain 
laurel, paraquat, parathion, Portuguese man-of- 
war, potato, privet, rhubarb, rotenone, scorpions, 
spindle tree, stibine, stingray, tetrachloroethane, 
Thyrolar, turpentine, Vacor, water hemlock, yew 

Appetite Loss Bacillus anthracis (anthrax), 
Preludin 



202 poisons, by symptom 



Bloating Barbados nut 

Constipation opium, Percodan, Vacor, white 
snakeroot 

Cramps arsenic, castor bean, colocynth, elder- 
berry, iieroin, panther mushroom, pokeweed, scor- 
pions, stingray, TEPP 

Diarrhea (bloody) acid, Amanita mush- 
room, antimony. Bacillus anthracis (anthrax), bane- 
berry, colocynth, croton oil, daphne, fool's parsley, 
meadow saffron, mercury, moonseed, oleander, 
tetrachloroethane, warfarin 

Diarrhea alkalies, amphetamines, arsenic, 
Barbados nut, barium, benzene hexachloride, betel 
nut seed, black hellebore, boric acid, boron, bro- 
mates, bryony, cadmium, cantharidin, cinchophen, 
daffodil, digitoxin, false hellebore, fly agaric, form- 
aldehyde, foxglove, Gyromitra mushroom, hemlock, 
horse chestnut, Inderal, iodine, lead, malathion, 
mandrake, Minipress, mold, naphthalene, nicotine, 
panther mushroom, paraquat, parathion, paternos- 
ter pea, phosphorus, poinsettia, pokeweed, polo- 
nium-210, potato, privet, pyrethrum, quinidine, 
rhododendron, silver nitrate, spindle tree, Tagamet, 
TEPP, Thyrolar, tularemia, turpentine, water hem- 
lock, yew 

Nausea akee, aldrin, Amanita mushroom, 
amphetamines, antimony, arsenic. Bacillus anthra- 
cis (anthrax), baneberry, barium, benzene, black 
locust, black widow spider, boron, botuhsm, brown 
recluse spider, bryony, cadmium, camphor, can- 
tharidin, carbon monoxide, carbon tetrachloride, 
cassava, castor bean, Catapres, cationic deter- 
gents, celandine, cinchona bark, cobra, colum- 
bine, corn cockle, Cortinarius mushroom, daffodil, 
daphne, Depakene, dieldrin, digitoxin, dyphylline, 
ecstasy, elderberry, endrin, epinephrine, ergot, 
ethyl alcohol, ethylene chlorohydrin, false helle- 
bore, fly agaric, foxglove, Gila monster, grounsel, 
Halcion, hydrangea, hydrogen sulfide, Inderal, 
Indian tobacco, ipecac, isopropanol, larkspur, Lasix, 
lily of the valley, malathion, mercury, metha- 
nol, Minipress, monkshood, monoamine oxidase 
(MAO) inhibitors, morphine, mountain laurel, 
naphthalene, narcissus, nicotine, Norflex, opium, 
panther mushroom, parathion, paternoster pea, 
Percodan, Permitil, Persantine, persistent organic 
pollutants, phosphorus, pokeweed, polonium-210, 
privet, pyrethrum, quaalude, quinidine, rattle- 



snake, Reglan, rhododendron, rhubarb, Ritalin, 
rotenone, selective serotonin reuptake inhibitors, 
shellfish poisoning, stibine, stingray, Talwin, tang- 
hin, tetrachloroethane 
Stool (dark) lead 

Vomiting acid, akee, aldrin, alkalies, Amanita 
mushroom, ammonia, amphetamines, antimony, 
arsenic, atophan, baneberry, Barbados nut, barium, 
benzene, benzene hexachloride, betel nut seed, 
black locust, black widow spider, bloodroot, blue 
ringed octopus, boric acid, boron, bromates, bron- 
chial tube relaxers, brown recluse spider, bryony, 
cadmium, caffeine, camphor, cantharidin, carbon 
tetrachloride, cassava, castor bean, celandine, cin- 
chona bark, cocaine, columbine, Cortinarius mush- 
room, croton oil, daphne, DDT, dieldrin, digitoxin, 
dog mercury, dyphylline, epinephrine, ergot, ethyl 
alcohol, ethylene chlorohydrin, false hellebore, 
formaldehyde, foxglove, grounsel, Gyromitras mush- 
room, Halcion, hemlock, horse chestnut, Inderal, 
Indian tobacco, insulin, iodine, ipecac, ketamine, 
larkspur, Lasix, lead, lily of the valley, malathion, 
mandrake, meadow saffron, mercury, Minipress, 
monkshood, monoamine oxidase (MAO) inhibitors, 
mountain laurel, naphthalene, narcissus, nicotine, 
nitroglycerine, Norflex, oleander, opium, paraquat, 
Percodan, petroleum distillates, phosphorus, phy- 
sostigmine, poinsettia, pokeweed, polonium-210, 
potato, privet, pyrethrum, quaalude, rattlesnake, 
rhododendron, rhubarb, Ritalin, rotenone, savin, 
selective serotonin reuptake inhibitors, shellfish 
poisoning, silver nitrate, sodium fluoroacetate, 
spindle tree, stingray, Tanghin, TEPP, toxaphene, 
turpentine, Tylenol, Vacor, water hemlock, white 
snakeroot, yew 

Stupor 

aniline, black locust, castor bean, Indian tobacco, 
Inocybe mushroom, iodine, monoamine oxi- 
dase (MAO) inhibitors, PCP, Percodan, potato, 
rotenone 

Unconsciousness 

benzene, camphor, carbon fumes, carbon monox- 
ide, carbon tetrachloride, chloral hydrate, cocaine, 
codeine, cyanide, Dalmane, endrin, ether, ethyl 
alcohol, ethylene chlorohydrin, formaldehyde, 
heroin, hydrangea, hydrogen sulfide, Inocibe mush- 



poison sumac 203 



room, marijuana, Minipress, morphine, oleander, 
opium, petroleum distillates, stonefish, trichloro- 
ethane, turpentine, Valium 

Urinary Tract Problems 

Lack of Urine atropine, belladonna, black 
widow spider, bromates, colocynth, cort mush- 
rooms, Elavil, ergot, iodine, meadow saffron, rhu- 
barb, savin, silver nitrate, tansy, trinitrotoluene 

Dark Color flagyl, phenol 

Painful Urination Barbados nut, naphtha- 
lene, turpentine 

Frequent Urine Lasix, Vacor 

Urinary Retention aspirin, atropine, bella- 
donna, benzylpiperazine, black widow spider, bro- 
mates, colocynth, flunitrazepam, isopropanol, lead, 
naphthalene, paraquat, savin, trinitrotoluene 

Uremia aldrin, aspirin, brown recluse spider, 
cantharidin, carbon tetrachloride, castor bean, cort 
mushrooms, dieldrin, iodine, mercury, naphtha- 
lene, savin, turpentine, warfarin 

Yellow Urine atophan 

Visual Problems 

Blindness ammonia, atropine, hemlock, jim- 
sonweed, methanol, phenol, propane 

Blurry/Double Vision alkalies, atropine, 
beaked sea snake, belladonna, benzene, betel nut 
seed, botulism, cinchona bark, digitoxin, dimethyl 
sulfate, ecstasy, Elavil, epinephrine, ethyl alco- 
hol, false hellebore, fool's parsley, foxglove, Hal- 
dol, hemlock, henbane, heroin, hydrogen sulfide, 
jimsonweed, Lasix, Librax, malathion, methanol, 
Minipress, monkshood, nicotine, Norflex, panther 
mushroom, Permitil, Tanghin, TEPP, Vacor 

Dilated Pupils atropine, belladonna, ben- 
zylpiperazine, bloodroot, cocaine, Elavil, epineph- 
rine, ethyl alcohol, heroin, horse chestnut, Indian 
tobacco, lily of the valley, parathion, tansy, water 
hemlock, yellow jessamine, yew 

Pinpoint Pupils morphine, opium, physo- 
stigmine, TEPP 

Reddened Eyes dimethyl sulfate, hydrogen 
sulfide 

Sensitivity to Light atropine, Lasix, parathion 
Teary Eyes dimethyl sulfate, fly agaric mush- 
room, formaldehyde, malathion, mountain laurel, 
panther mushroom, rhododendron, TEPP 



poison sumac (Toxicodendron, vernix [L.] Kuntzel 
[= Rhus vernix L.]) This poisonous tree, a relative 
of poison ivy and poison oak, has seven to 1 3 long, 
narrow leaves growing in pairs with a single leaf at 
the end of the stem. In the spring, the leaves are 
bright orange and look something like velvet; as 
the season progresses, they become dark green and 
glossy on the upper surface of the leaf and light 
green on the underside. In the fall, the leaves turn 
red or orange. Poison sumac can be differentiated 
from nonpoisonous sumacs by its drooping clusters 
of green berries — nonpoisonous sumacs have red, 
upright clusters of berries. Poison sumac can grow 
to be 25 feet tall, although it more often reaches 
heights of five to six feet. It is found in swampy 
areas throughout eastern United States. 

Symptoms 

Symptoms vary from one person to the next, rang- 
ing from mild itching to severe burning and itching 
with watery blisters, and usually develop within 
24 to 48 hours in a sensitive person. Symptoms 
usually peak about five days after contamination 
and gradually improve over a week or two even 
without treatment. Eventually, the bhsters break, 
and the oozing sores crust over and then disappear. 
The poison sumac rash is not spread by scratch- 
ing open blisters but by the urushiol found in the 
plant. Anything that brushes against this oil is 
contaminated and can pass on the rash if it brushes 
the skin. For this reason, doctors recommend not 
scratching blisters, since any remaining urushiol 
that hasn't been washed off can be transmitted to 
another part of the body. Animals can also transmit 
poison sumac from their fur to their owners's skin. 
Any animal suspected of coming in contact with 
poison sumac should be given a bath; gloves should 
be worn while bathing. 

Treatment 

The best treatment is to wash the affected area 
immediately after contact with yellow laundry 
soap and cold water, lathering several times and 
rinsing the area in running water after each suds- 
ing. Do not scrub with a brush. If contaminated 
while in isolated areas, wash in a cold running 
stream. Any clothing that might have come in con- 
tact with urushiol must be washed several times. 



204 poisonwood 



If the urushiol is washed off the skin, there is httle 
further treatment needed in mild cases. Itching can 
be treated with compresses soaked in cold water, 
and calamine lotion spread over the rash will help 
relieve the itching and burning. In the case of a 
severe reaction, a physician may prescribe cortico- 
steroid drugs by mouth or injection. 
See also poison ivy; urushiol. 

poisonwood (Metopium toxiferum) One of a 

group of plants that are poisonous on contact, 
poisonwood is found in southern Florida to the 
Bahamas, Honduras, and the West Indies. It is 
related to poison oak and poison sumac, which 
places it in the Anacardiaceae family. Anyone who 
lives or works in southern Florida should learn to 
recognize poisonwood because any contact with it 
causes a negative reaction. Poisonwood is found 
in pinelands, sandy dunes near salt water, and in 
hammocks. The plant has a yellow-orange fruit 
that is enjoyed by many birds and animals. 

Poisonous part 

The sap contains alkaloids that cause a toxic effect 
on contact with the skin. Since any part of this tree 
can carry the sap, contact with any part of the poi- 
sonwood tree can be poisonous. 

Symptoms 

Upon contact, the individual's skin turns black and 
a rash and blisters develop. Smoke from a burning 
tree can cause temporary blindness. 

Treatment 

Symptomatic. According to folk medicine, the sap 
of another tree indigenous to the same area, the 
gum elemi or gumbo-limbo tree (Bursera simaruba), 
is an antidote to the sap of the poisonwood. 

pokeweed (Phytolacca americana) [Other names: 
American nightshade, cancer jalap, crow berry, 
Indian polk, inkberry, pigeon-berry, pocan bush, poke, 
pokeberry, red ink plant, red weed, scoke.] This 
unpleasant-smelling plant is found in damp, woodsy 
areas from Maine to Minnesota, south to the Gulf 
of Mexico, Florida, and Texas and also in California 



and Hawaii; it can also be found in parts of Canada, 
Europe, and southern Africa. It is commonly found 
along fields and fences, growing 12 feet tall with 
white to purple drooping flowers, black berries, and 
a large perennial rootstock. Young leaves and stems 
are sometimes eaten as cooked greens, and these 
can be eaten safely if cooked twice in two different 
pans of water. 

Poisonous part 

All parts of the pokeweed plant contain the poison 
laccine, saponins, and glycoproteins, especially the 
roots and leaves — and the seeds are almost as toxic 
as the roots. Only two or three unripe berries can 
be fatal if eaten by a child, although mature berries 
are relatively nontoxic. Poisonings usually occur 
from eating uncooked leaves in salads or by mis- 
taking the roots for parsnips or horseradish. 

Symptoms 

Symptoms begin about two hours after inges- 
tion and include burning and bitterness in the 
mouth, nausea, vomiting and diarrhea; occasion- 
ally, spasms, convulsions, and death occur. 

Treatment 

Gastric lavage; replacement of fluids and 
electrolytes. 

See also saponin. 



polonium-210 At the end of the 19th century, 
Marie Curie discovered polonium-210, a radioac- 
tive material that occurs in nature at very low 
levels as part of the decay of uranium and from 
lead-containing wastes from uranium, radium, 
and vanadium refining. Polonium-210 also can 
be produced artificially in nuclear reactors, which 
requires highly skilled individuals and sophisti- 
cated equipment to do so. Nearly all of the world's 
legal polonium-210 is produced in Russia. 

Polonium-2 10 emits alpha particles that are 5,000 
times more radioactive than radium. These particles 
carry high amounts of energy that can damage or 
destroy genetic material in the body. Industrially, 
polonium-210 is used to eliminate static electricity 
in processes such as manufacturing sheet plastics, 
spinning synthetic fibers, and rolling paper. It is also 



polychlorinated biphenyls 205 



used to make nuclear weapons, power supplies in 
satellites, and in the oil industry. 

Polonium-210 poses a radiation hazard only if 
it enters the body, either through eating, a break 
in the skin, or through breathing. Once inside the 
body it irradiates the internal organs, which can 
result in life-threatening symptoms or death. Polo- 
nium-210 is not harmful if it touches unbroken 
skin or membranes, although it is recommended to 
wash any areas that have been exposed. 

Polonium-210 hit headlines around the world 
in 2006 when Alexander Litvinenko, a former 
officer of the Russian Federal Security Service who 
had received political asylum in Great Britain, was 
poisoned with the material while dining at a British 
eating establishment. He died within three weeks 
of ingesting the polonium and was the first known 
victim of lethal polonium-210 caused acute radia- 
tion syndrome. 

Symptoms 

Within 48 hours of exposure, symptoms include 
nausea, vomiting, and diarrhea. If a large dose 
enters the gut, it can cause bone marrow failure 
which manifests as nosebleeds, bleeding gums, 
bruising, and sudden hair loss two to four weeks 
after exposure. At high doses, polonium-210 can 
damage tissues and organs such as kidneys, spleen, 
liver, and bone marrow. As it travels throughout 
the body in the blood it damages all cells it encoun- 
ters, eventually leading to death. 

Treatment 

There is no antidote or cure for polonium-210 poi- 
soning. Treatment is symptomatic. At lower doses, 
intense antibiotic therapy, bone marrow transplant, 
and chelation may be beneficial if the poisoning is 
diagnosed quickly. 

polychlorinated biphenyls (PCBs) This group 
of up to 209 individual chlorinated compounds 
(called congeners) are no longer produced in the 
United States, as the Environmental Protection 
Agency (EPA) banned their manufacture in 1977 
because of evidence that they may cause cancer 
and other serious health problems in humans. 
They are known to produce cancer in animals. 



PCBs are either oily liquids or solids that are 
colorless to light or dark amber. Some PCBs exist 
as vapor in air. Although PCBs were banned 
decades ago, they continue to cause problems in 
the environment because they have a long half- 
life, are very stable, and are readily taken up by 
living organisms. Before 1977, PCBs were used as 
coolants and lubricants in transformers, capacitors, 
and other electrical equipment because they are 
good insulators. Many of these items that once 
contained PCBs have leaked the substance into the 
environment, making PCB contamination almost 
universal. PCBs also entered the environment 
from accidental spills, from fires in products that 
contained the toxins, and from leaks that occurred 
during their transport. Today these toxins are still 
being released from hazardous waste sites, from 
improper or illegal disposal of consumer and indus- 
trial products, and from the burning of some waste 
in incinerators. 

Once PCBs reach the environment, they can 
exist for many years and they can travel great 
distances in the air and by water. PCBs in water 
usually stick to organic particles and sediment and 
also bind strongly to soil. Fish and other marine 
mammals take up PCBs and accumulate the tox- 
ins in their bodies, passing them along to other 
animals or humans who eat them. For these and 
other reasons, PCBs are still found in human milk, 
in human fat tissue, and in the brain and liver of 
young children. 

In 2008, the French-owned waste management 
company, Veoha Environmental Services, in Port 
Arthur, Texas, petitioned the EPA for permission to 
burn 40 million pounds of PCBs from Mexico in its 
plant. The plant has been disposing of PCB waste 
from the United States since 1992. The EPA gave 
tentative approval to the proposal in March 2008, 
and a final decision was expected by the second 
half of 2009. 

Currently, the EPA has set a limit of 0.0005 mil- 
hgrams of PCBs per liter of drinking water. Any 
spill, discharge, or accidental release of one pound 
or more of PCBs into the environment must be 
reported to the EPA. The acceptable amount of 
PCBs in food is determined by the Food and Drug 
Administration, which states that no more than 
0.2-0.3 parts of PCBs per million parts (0.2-0.3 



206 Portuguese man-of-war 



ppm) can be contained in infant foods, eggs, milk 
and otfier dairy foods, fisfi, sfiellfish, poultry, and 
red meat. Many individual states have fish and 
wildlife consumption advisories for PCBs. 

Symptoms 

PCBs are readily taken up by the body, when 
inhaled, ingested, or absorbed through the skin. 
They are also well absorbed from the gastrointes- 
tinal tract and are stored in fat. Both skin contact 
and ingestion cause the skin disease chloracne, 
liver damage, skin hyperpigmentation, blindness, 
swelling, nausea, vomiting, and abdominal pain. 
PCBs are far more likely to cause poisoning as a 
result of long-term exposure rather than with a 
single acute overdose. Chronic exposure may cause 
symptoms as much as six weeks or longer after the 
onset of exposure. 

Treatment 

There is no way to remove PCBs once they have 
entered the body. Treatment is supportive and 
symptomatic, aimed at preventing liver damage. If 
inhaled, give supplemental oxygen. Wash contami- 
nated skin or eyes; if ingested, induce vomiting or 
perform gastric lavage followed by the administra- 
tion of activated charcoal and a cathartic. 
See also saponin. 



Portuguese man-of-war (Physalia physalis) A 

well-known member of the jellyfish family, the 
Portuguese man-of-war (also known as a blue- 
bottle) gets its name from the floating portion of its 
body that appears above the surface of the ocean 
and resembles the rigging of a caravel. Technically, 
the Portuguese man-of-war is not a jellyfish but 
a hydroid — a colony that consists of four types of 
polyps: a pneumatophore, or float; dactylozooids, 
or tentacles; gastrozooids, or feeding zooids; and 
gonozooids, which produce reproductive cells. 

Poisonous part 

The tentacles of the Portuguese man-of-war trail 
several feet below its body, floating on the sur- 
face of the water; some tentacles will be mark- 
edly longer than the others and are called "fishing 
tentacles." These poisonous tentacles may extend 



from the central float bag for 50 feet or more. All 
the tentacles are covered with many thousands of 
stinging cells that emit a coiled hoUow thread that 
can penetrate skin. Venom in these coils is injected 
through the thread. The man-of-war is found 
throughout the world in warm waters, and its sting 
is far more severe than those from the more com- 
mon jellyfish. 

Symptoms 

Toxicity depends on the sensitivity of the victim 
and the number of stings. Symptoms include 
immediate and intense stinging or throbbing, a 
radiating sensation similar to being stung by hor- 
nets, causing wheals and blisters, severe chest and 
abdominal pain, shock, and collapse. The pain has 
been compared to an electric shock, with the sen- 
sation extending up the extremity. More general- 
ized symptoms include headache, shock, cramps, 
nausea, and vomiting, and recent reports have 
noted the possibility of acute kidney failure. 

Treatment 

There is no known specific antidote. At one time, 
the recommended way to deactivate the tentacles 
was to pour alcohol, ammonia, vinegar, or salt 
water over the stings, after which they could be 
scraped off with a towel. Now, however, it's been 
discovered that vinegar causes the nematocysts 
(coiled threadlike structures) to discharge a toxin. 
In smaller species of jellyfish, vinegar inhibited 
some nematocysts but discharged others. Alcohol 
also has been shown to cause a massive discharge 
of toxin in a similar species of jellyfish and so is 
no longer recommended. Studies that have looked 
at the effectiveness of baking soda, papain, meat 
tenderizer, and commercial sprays that contain 
aluminum sulfate and detergents have been incon- 
clusive, and it is possible that these substances can 
cause further damage. 

The suggested course of treatment includes: (I) 
gently pick off any visible tentacles using a stick, 
gloved hand, or anything that does not promote 
further injury; (2) rinse the sting thoroughly with 
fresh or salt water; (3) apply ice to control pain; (4) 
for rash or persistent itching, use I percent hydro- 
cortisone ointment four times daily and one or two 
25-mg diphenhydramine tablets every six hours. 



potato 207 



Because the tentacles will continue to discharge 
their nematocysts as long as they remain on the 
skin, it is critical to remove them. Stung individuals 
should be watched carefully for signs of shock or 
breathing difficulties. 

See also jellyfish. 

potassium hydroxide See alkaline corrosives. 

potassium or sodium thiocyanate This drug, tra- 
ditionally given for high blood pressure, has been 
replaced by safer drugs, although sodium thiocya- 
nate is still prescribed by a few physicians. 

Symptoms 

Almost immediately upon ingestion of large 
amounts, the drug begins to depress cellular activ- 
ity of the heart and brain, causing disorientation, 
weakness, low blood pressure, confusion, psychotic 
behavior, convulsions, and death. Even when the 
victim begins to recover from thiocyanate poison- 
ing, death can still occur after a sudden relapse as 
much as two weeks after poisoning. 

Treatment 

Perform peritoneal dialysis. 

potassium permanganate A disinfectant and 
mild antiseptic with astringent properties that can 
be used to treat skin inflammation and wounds, 
potassium permanganate may be applied to a dress- 
ing or directly to the skin. It is sometimes used to 
treat strychnine, nicotine, and quinine poisoning, 
although it is always hazardous to use. Care needs 
to be taken when mixing the crystals in water, 
because if the mixture is too concentrated (greater 
than one to 5,000 parts strength), the solution 
will cause corrosive burns and destroy the mucous 
membranes. Potassium permanganate tablets (400 
mg, 1:1,000) are commonly used in clinical prac- 
tice, and they are diluted in four liters of water to 
reach a safe dilution of 1:10,000. 

Some women have used potassium perman- 
ganate to induce abortion by inserting it into the 
vagina, and the result has been massive hemor- 
rhaging and serious injury to the vaginal walls. 



Symptoms 

While symptoms vary depending on the dose, low 
concentrations cause a burning feeling in the throat, 
nausea, vomiting, difficulty in swallowing, and 
some gastroenteritis. In stronger concentrations (2 
or 3 percent solutions), symptoms will also include 
swollen throat and dry mouth, making swallow- 
ing difficult. At even greater concentrations (4 to 5 
percent), kidney damage will occur and there may 
be possible disorientation, low blood pressure, and 
rapid, shallow pulse; death may follow from circu- 
latory failure or pulmonary complications. 

Treatment 

In cases of skin contamination, wash affected area 
repeatedly with warm tap water, and treat perfo- 
rations surgically. For ingestion, do NOT induce 
vomiting; perform gastric lavage cautiously. Acti- 
vated charcoal and cathartics are not useful. Give 
large amounts of fluid and supportive therapy. Cold 
milk is also suggested as a way to oxidize organic 
material. 

See also nicotine; quinine; strychinine. 



potato This cousin of deadly nightshade is a 
popular vegetable throughout the world, but it can 
be poisonous if eaten raw and unripe. Although 
the skin of a potato has more fiber, iron, potas- 
sium, and B vitamins than the flesh, skins that 
have a greenish tinge should be avoided, as this 
signals the presence of chlorophyll, a sign that the 
potato was exposed to too much light after harvest. 
Chlorophyll alone is harmless, but in potatoes, the 
green indicates the presence of glycoalkaloids, and 
in this case, a toxin called solanine. Ultraviolet and 
visible light in the blue-violet region promotes the 
formation of glycoalkaloids. High levels of solanine 
cause affected potatoes to taste bitter after they are 
cooked. Solanine formation in potatoes is limited 
to the skin and usually no deeper than an eighth 
of an inch into the flesh. 

Poisonous part 

The leaves, stems, skin, and sprouts of potatoes 
with greenish skin contain solanine, a naturally 
occurring glycoalkaloid, and other toxins. Although 
undamaged potatoes contain some solanine, the 



208 pothos 



concentration is very low and a person would have 
to eat about 12 pounds of them to be poisoned. If a 
potato has greenish skin, pare away the green areas 
and gouge out all sprouts. Solanine has a stronger 
effect on children. 

Symptoms 

A fast-acting toxin, solanine causes symptoms 
including burning and rawness in the throat, head- 
ache, vomiting, abdominal pain, diarrhea, swelling 
of the brain, stupor, coma, convulsions, and death 
(usually in children). 

Treatment 

Gastric lavage, cathartics, and fluid and electrolyte 
monitoring. 

See also nightshade, deadly. 

pothos (Epipremnum aureum) [Other names: dev- 
il's ivy, golden Ceylon creeper, golden hunter's 
robe, golden pothos, ivy arum, Solomon Island ivy, 
taro vine, variegated philodendron.] This popular 
indoor plant often found in hanging baskets grows 
outdoors throughout subtropical chmates of south- 
ern Florida, Hawaii, Guam, and the West Indies, 
where it twines on trees up to 40 feet high. 

Poisonous part 
The entire plant is toxic and contains calcium oxa- 
late raphides and other, unidentified irritants. 

Symptoms 

Skin contact causes dermatitis, and ingestion by 
children results in diarrhea. 

Treatment 

There is no specific treatment, but guard against 
dehydration in children with diarrhea. 
See also oxalates. 

pralidoxime This drug is used as an antidote to 
organophosphate insecticide poisoning and is most 
effective if treatment is begun within 24 hours 
after exposure. Its use in the treatment of carba- 
mate poisoning is still controversial; it may not be 
harmful, but it is not often used because of its short 
duration. 



See also carbamate; organophosphate 

INSECTICIDES. 

Preludin (phenmetrazine hydrochloride) One of 

the appetite-suppressant drugs of high toxicity, 
Preludin is a white water-soluble powder and is 
available in tablets or injectables. Similar to amphet- 
amines, Preludin activates the central nervous sys- 
tem and raises blood pressure; rapid heartbeat and 
addiction are quite common. Within a few weeks or 
using this drug, tolerance begins to develop. 

Symptoms 

Appetite suppression, impaired judgment, incoor- 
dination, palpitations, high blood pressure, rest- 
lessness, dizziness, dry mouth, euphoria, insomnia, 
tremors, confusion, headache, hallucinations, 
panic, fatigue, and depression. Psychotic episodes 
are possible even at recommended doses, together 
with an unpleasant taste in the mouth, diarrhea or 
constipation, and other stomach problems. Over- 
dose may cause circulatory collapse, coma, high 
or low blood pressure followed by death. Abruptly 
stopping the drug causes depression, fatigue, irri- 
tability, hyperactivity, and psychosis (sometimes 
confused with schizophrenia). 

Treatment 

Sedation with barbiturates. 
See also amphetamines. 

privet (Ligustrum vulgare) This common hedge 
plant is a deciduous shrub with small, white clus- 
tering flowers and blue or black waxy berries that 
appear throughout the winter. Native to the Medi- 
terranean, privet hedges are grown throughout the 
United States and Canada. 

Poisonous part 

The entire plant, including the berries, contains the 
irritant glycoside syringin (ligustrin), nuzhenids, 
and secoiridoid glucosides. 

Symptoms 

A large number of berries can cause diarrhea, colic, 
and gastroenteritis; poisoning can be fatal in young 
children. 



Prunus 209 



Treatment 

Fluid replacement to prevent dehydration. 

procaine A local anesthetic and related to cocaine, 
this drug is a synthetic version of the coca bush 
alkaloids. It is used to control possible irregular 
heartbeat following poisoning by a variety of car- 
dioactive drugs and toxins (such as digoxin, cyclic 
antidepressants, stimulants, and theophylline). It 
is also used to relieve pain and irritation caused by 
sunburn or hemorrhoids, to numb tissues before 
minor surgery and as a nerve block. It is used topi- 
cally to relieve pain when inserting needles, and it 
is given intravenously as an antiarrhythmic agent 
following a heart attack to reduce the danger of 
ventricular arrhythmias (irregular heartbeat). 

Although procaine is used to treat poison- 
ing by other drugs, it is also toxic itself if used 
excessively. 

Symptoms 

Immediately upon ingestion, procaine causes gid- 
diness followed by dizziness, blue color, low blood 
pressure, tremors, irregular and weak breathing, 
collapse, coma, convulsions, and respiratory arrest. 
Procaine is considered to be the most dangerous of 
all the cocaine derivatives; even a small amount 
can cause fatal shock. 

Treatment 

Efforts to remove the drug after 30 minutes 
are useless. The ingested drug must be removed 
immediately and absorption from the injection site 
limited by tourniquet and wet cloths. Give oxygen 
and artificial respiration until the nervous system 
depression lifts. If the victim survives for one hour, 
recovery outlook is good. 

See also anesthetics, local; cocaine; digoxin; 

LIDOCAINE. 



propane The principal ingredient in bottled gas 
in northern states, which (in low concentrations) 
is physiologically inert. However, high concentra- 
tions of the gas may cause narcosis (a state of sleep 
or drowsiness). A concentration of 10 percent 
propane causes slight dizziness in a few minutes; 



displacement of air by this gas can cause short- 
ness of breath, unconsciousness, and death. The 
principal toxic effects from gases are from carbon 
monoxide. 

See also carbon monoxide. 



propranolol This beta adrenergic blocker is used 
to control heart irregularities caused by overdose of 
theophylline, caffeine, amphetamines, ephedrine, 
or cocaine. 

See also amphetamines; caffeine; cocaine; 
ephedrine; theophylline. 



Prunus A genus of trees and shrubs that includes 
apricot, cherry, choke cherry, peach, plum, and 
sloe, whose chewed pits are poisonous and possess 
cyanogenic glycosides. The Prunus species have 
white or pink flowers and a fleshy fruit over a 
stone or pit. They are widely cultivated throughout 
the northern temperate zone, and a large number 
of these fruit trees are available commercially. 

Poisonous part 

The kernel of the pit is poisonous, as it contains 
the cyanogenic glycosides (amygdalin) that liberate 
hydrocyanic acid on hydrolysis. Of all the poison- 
ings associated with the entire genus, the most fatal 
cases involve ingestion of apricot pits. 

Symptoms 

Hours may pass between ingestion of the pit and 
toxic symptoms, because the glycosides must be 
hydrolyzed in the gastrointestinal tract before 
cyanide is released. Once this occurs, symptoms 
include abdominal pain, vomiting, lethargy, and 
sweating. Cyanosis (blueness of the skin) may or 
may not occur. In severe cases, the victim may 
lapse into a coma and experience convulsions, flac- 
cid muscles, and incontinence. 

Treatment 

If the patient is conscious, perform gastric lavage. 
Although activated charcoal absorbs cyanide, it 
releases it slowly during its passage through the 
intestine; instead, give a 25 percent solution of 
sodium thiosulfate after lavage. If unconscious. 



210 Psilocybe mexicana 



correct acidosis, treat for shock and administer oxy- 
gen; administer cyanide antidote. 
See also cyanogenic glycosides. 



Psilocybe mexicana See Mexican hallucino- 
genic MUSHROOM. 



psilocybin One of tfie active substances found 
in a range of hallucinogenic mushrooms such as 
Psilocybe cubensis, Panaeolus subbalteatus, and Gym- 
nopilus spectabilis. Psilocybin primarily affects the 
levels of a brain transmitter known as serotonin; 
this effect is similar to the activities of mescaline 
or LSD. It commonly has an impact on the senses, 
particularly intensifications of color perception 
and "kaleidescope effects" with eyes closed. Mood 
alteration is also common, ranging from elation 
to anxiety, as are feelings of paranormal occur- 
rences, such as the sensation of leaving the body 
or traveling through time. The sensations usually 
last between four and 10 hours, and there are no 
lingering effects. 

See also hallucinogenic mushrooms; Mexican 

HALLUCINOGENIC MUSHROOM. 



ptomaine poisoning Ptomaines are substances 
produced by decaying animal or vegetable pro- 
teins; ptomaine poisoning is not the same as food 
poisoning. Foods that contain ptomaines are far 
from appetizing; they look, smell, and taste com- 
pletely unpleasant and therefore are not usually a 
danger to humans. Most ptomaines aren't harm- 
ful; most ptomaine poisoning is actually staphy- 
lococcal poisoning. Ptomaine poisoning is also an 
obsolete term for food poisoning caused by bacte- 
rial poisons. 

pufferfish This exotic food fish, considered a 
dehcacy in Japan where it is known as "fugu," 
can cause poisoning if improperly prepared and 
cooked. It can also inflict a painful sting. There are 
more than 120 species of puffer, all belonging to 
the family Tetraodontidae; they are considered to 
be one of the most poisonous fish in the world. 



with a 60 percent fatality rate even with treatment. 
In Japan, there are about 50 deaths a year; at least 
three have been reported in Florida. Pufferfish is 
still the primary cause of death from food poison- 
ing in Japan. From 1955 to 1975, 3,000 Japanese 
were poisoned by eating fugu and 1,500 died. 

Three cases of tetrodotoxin poisoning occurred 
among chefs in California in April 1996, when 
they shared contaminated pufferfish brought from 
Japan by a coworker as a prepackaged, ready-to- 
eat product. The amount that each chef ate was 
very small, ranging from about a quarter to half 
an ounce. Symptoms began between three and 20 
minutes after eating the fish, and all three people 
were transported by ambulance to a local emer- 
gency department. 

In Japan, cooks and restaurants that serve fugu 
must have a special license and training to prepare 
this sometimes deadly dish. Still, about 10 Japanese 
diners die each year from eating the wrong parts 
of the fish. Fugu lovers say that the fish tastes Hke 
chicken and that it produces a mild intoxication, 
feelings of warmth, and euphoria. In the United 
States, one species of puffer (called the blowfish) 
is served in restaurants under the name of "sea 
squab." 

Pufferfish get their name from their ability 
to inflate themselves when threatened, puffing 
themselves up to several times their normal girth 
until they are almost spherical. Puffers are most 
toxic just before and during their reproductive 
season, because of the interaction between gonad 
activity and toxicity, although the same species 
found in different locations at the same time could 
vary widely in its toxicity. They are commonly 
found in warm or temperate regions around the 
world, including the west coast of Central America, 
throughout the Indo-Pacific, Japan, and from Aus- 
tralia to South America. 

Puffers are very territorial and seek rocky crev- 
ices to hide in. A close relative is the deadly porcu- 
pine fish, which not only inflates when threatened 
but also erects sharp quills all over its body. 

Although it is against the law for an individual 
to bring pufferfish into the country, the U.S. Food 
and Drug Administration has allowed pufferfish to 
be imported and served in Japanese restaurants by 
certified fugu chefs on special occasions. A coop- 



pyrethrin 211 



erative agreement with the Japanese Ministry of 
Health and Welfare ensures fugu is properly pro- 
cessed and certified safe for consumption before 
export by the government of Japan. If cleaned and 
dressed properly, the puffer flesh or musculature 
is edible. 

Although arriving travelers are required to 
declare all food products brought into the United 
States, control measures rely primarily on the trav- 
eler. People who travel to countries where puffer 
is served should be aware of the potential risk of 
eating this fish. 

Poisonous part 

The liver, gonads, intestines, and skin of these fish 
contain tetrodotoxin, a powerful neurotoxin that 
can cause death in approximately 60 percent of 
persons who ingest it. Other animals, such as the 
California newt and the eastern salamander also 
have tetrodotoxin in lethal quantities. Tetrodo- 
toxin is a basic compound that does not deactivate 
when heated. This nerve poison is 150,000 times 
more deadly than curare. There is evidence that 
the toxin is included as part of the Haitian voodoo 
potion used in the zombie ritual. 

Symptoms 

While death from a puffer sting is rare, it causes 
an immediate severe throbbing pain that may stay 
at the site of the wound or spread throughout the 
body and last for several hours or days. There may 
be redness and swelling at the site of the sting, and 
the area may become numb. 

Improperly preparing or cooking this fish causes 
a far more serious type of poisoning. Within min- 
utes to hours, symptoms include numbness and 
tingling beginning in the extremities and spread- 
ing over the body together with a floating feeling. 
Other symptoms include fatigue, headache, tight- 
ness in throat and upper chest, speech problems, 
flushing, shaking, nausea, and vomiting. Paralysis 
in an ascending pattern appears, and the victim 
finds it difficult to breath, which progresses to 
coma, convulsions, respiratory arrest, and death. 
The first 24 hours after ingestion are critical; there 
is a high fatality rate. Severe poisoning causes 
symptoms of low blood pressure, slow heart rate, 
and fixed dilated pupils. 



Diagnosis 

Tetrodotoxin poisoning is diagnosed based on 
symptoms and a history of recent consumption of 
pufferfish. 

Treatment 

For a puffer sting, contact medical help immediately; 
flush the wound with fresh or salt water and then 
soak the affected area in hot water or put hot com- 
presses on it. The water should be very hot (I22°F), 
so that the heat will deactivate the poison. Continue 
applying hot water for 30 minutes to an hour. 

There is no antidote to tetrodotoxin ingestion, 
and there is great controversy over the relative 
benefits of the administration of atropine, edro- 
phonium, or pyridostigmine. Otherwise, treatment 
is supportive. Induce vomiting or perform gastric 
lavage if ingestion occurred within the preceding 
hour, followed by the administration of activated 
charcoal. Intravenous fluids may be helpful. 

See also tetrodotoxin. 



pyrethrin The active chemical derived from pyre- 
thrum (extracted from chrysanthemums grown 
in the Democratic Republic of Congo and Kenya), 
pyrethrin is one of the oldest known botanic insec- 
ticides. It was used hundreds of years ago in China, 
and the plants were cultivated in Europe more than 
a century ago. Pyrethrin and pyrethrum come from 
two strains of chrysanthemum (roseum and car- 
neum). To make the insecticide, pyrethrum flow- 
ers are ground and then used either undiluted or 
mixed with inert ingredients or other insecticides to 
kill a variety of garden and household insect pests. 

While pyrethrin has largely been replaced by 
more toxic insecticides, it is still often found in 
pesticide preparations for fighting fleas in dogs. 
Both pyrethrum and pyrethrin are the most widely 
used natural insecticides because they are deadly 
to a wide range of insects — possibly as effective 
in controlling pests as Sevin (carbaryl), a popular 
synthetic pesticide. 

Pyrethrin is stronger than its dried flower source, 
since it has been strengthened to prevent insects 
from recovering from the effects of the poison. 
These substances are somewhat controversial today 
because in large quantities they can affect the 



212 pyrethrum 



human nervous system. They can kill or incapaci- 
tate beetles, caterpillars, flies, wasps, bees, moths, 
fruit flies, butterflies, borers, whiteflies, chafers, 
leaf rollers, and many other insects. 

Symptoms 

Breathing pyrethrin causes the most toxic reaction 
because of its highly allergic properties; skin contact 
can cause dermatitis in about half of those sensi- 
tive to ragweed. Severe poisoning with pyrethrin 
is unusual, although it can cause nausea, vomiting, 
gastroenteritis, excitability, incoordination, muscular 
paralysis, and death from respiratory failure. Symp- 
toms may last between two days and two weeks. 
Less serious poisoning results in reddened skin, 
burning, and itching, swollen cheeks, headache, 
stomach problems, and numb lips and tongue. 

Treatment 

Atropine therapy may control gastroenteritis. Wash 
pyrethrin from eyes and skin, as it can cause a 
severe local dermatitis. Treat symptoms. 
See also botanic insecticides; pyrethrum. 



pyrethrum A wide-spectrum botanic insecticide 
used for hundreds of years in China, pyrethrum is 
a powder made from one of two forms of chrysan- 
themums (roseum and carneum). Pyrethrin is the 
active chemical derived from pyrethrum and is also 
used as an insecticide. 

Pyrethrum is a widely used natural insecticide 
because it can kill a wide variety of insects while 
posing little harm to humans and animals. Pyre- 
thrum is more benign than its chemical ester pyre- 
thrin and breaks down much faster (usually within 
24 hours). It does not kill some insect pests but 
only stuns them for a period of time. 

See also botanic insecticides; pyrethrin. 

pyridoxine (Vitamin Bg) See vitamins. 



Quaalude (methaqualone) An antianxiety drug 
introduced in 1965 as a safe barbiturate substitute, 
helpful in relieving anxiety and tension and as a 
sleeping pill. Experience showed, however, that 
Quaalude was very addictive and the severity of 
withdrawal symptoms was similar to that of barbi- 
turates. By 1972, "luding out" (taking methaqua- 
lone with wine) was a popular college pastime. 

In the United States, the marketing of methaqua- 
lone pharmaceutical products stopped in 1984, and 
methaqualone was transferred to Schedule I of the 
Controlled Substance Act, the highest designation 
of abuse potential. They are still available on the 
street as a drug of abuse. 

Symptoms 

Within five to 30 minutes, depending on whether 
the drug was injected or taken as a pill, symptoms 
of overdose appear; they include nausea and vom- 
iting, stomach irritation, pulmonary edema, con- 
vulsions, and death. 

Treatment 

Overdose is more difficult to treat than barbiturate 
overdose, and deaths have frequently occurred. 
Gastric lavage and treatment of symptoms are the 
only treatment. 

See also narcotics. 



quicklime (calcium oxide) Also called unslaked 
lime, this very powerful caustic is a component 
of Portland cement and liberates heat in contact 
with water. It can cause serious damage if ingested, 
inhaled, or allowed to contact the eyes. Note: 
Slaked lime (calcium hydroxide) is a simple alkali, 
and because of its low solubility in water, it is not 
greatly corrosive. 



Symptoms 

Contact with the skin may product first-, second-, 
or third-degree chemical burns; eye contact may 
produce severe conjunctivitis as well as damaged 
corneas. Ingestion produces burning pain from 
mouth to stomach, with marked difficulty in 
swallowing. Mucous membranes are soapy and 
white and then turn brown and become ulcer- 
ated. Vomit is bloody and may contain shreds 
of mucous membrane. Pulse is feeble and rapid, 
breathing is rapid, and collapse may follow. Death 
may result from shock, asphyxiation from swell- 
ing and intercurrent infections; pneumonia may 
occur in 48 to 72 hours. Esophageal stricture may 
develop within weeks, months, or even years after 
ingestion. 

Treatment 

Cold milk, water, or tea should be given immedi- 
ately. Irrigate the mouth with water; the damage to 
the esophagus from caustic alkalies occurs within 
the first minute, and therefore first aid measures 
after that are of doubtful value. DO NOT give 
carbonated beverages, and DO NOT induce vomit- 
ing or attempt gastric lavage (the small amount of 
alkali that usually reaches the stomach is quickly 
neutralized by the acid gastric juice). Olive oil may 
temporarily ease pain but should not be given in 
large amounts. 

See also alkaline corrosives. 



quinidine This is one of a group of antiarrhyth- 
mic drugs commonly used to control heartbeat 
irregularities and malaria and other infections. 
Acute ingestion of one gram of quinidine should be 
considered potentially lethal. 



213 



214 quinine 



Symptoms 

This drug primarily affects tfie cardiovascular and 
central nervous systems. Symptoms include heart 
problems, dry mouth, dilated pupils, delirium, 
seizures, coma, and respiratory arrest. In addition, 
there may be nausea, vomiting, and diarrhea after 
acute ingestion, and with chronic doses there may 
be tinnitus (ringing in the ears), vertigo, deafness, 
and visual disturbances. 

Treatment 

Most therapies have proven ineffectual, and there 
is no known antidote. The primary goal is to keep 
the heart functioning until the drug is eliminated, 
which usually occurs within a few hours. Heart 
problems are treated with hypertonic sodium bicar- 
bonate. Do not induce vomiting; perform gastric 
lavage followed by the administration of acti- 
vated charcoal and a cathartic. Quinidine is not 
effectively removed by dialysis. Treat low blood 
pressure, heart rhythm irregularities, coma, and 
seizures as they occur; treat recurrent rapid heart- 
beat with lidocaine or phenytoin. 
See also antiarrhythmic drugs. 

quinine A former drug treatment for malaria, 
quinine has largely been replaced by chloroquine 
but is still used for cases resistant to the newer 
drug. It is still prescribed for the treatment of noc- 
turnal muscle cramps and has also been used to 
induce abortions. The chief alkaloid of cinchona 
bark, quinine also contains related drugs (including 
quinidine). 

The quinine content of "tonic" water is usually 
no larger than 30 milhgrams per 100 milliliters. 



although this small amount can produce symptoms 
in very sensitive people. Dubonnet contains seven 
milhgrams per 100 milliliters. 

The mechanism behind quinine's toxicity is 
believed to be similar to that of quinidine, although 
quinine is much less toxic to the heart. It is avail- 
able in capsules and tablets of 130 to 325 milli- 
grams; the minimum toxic dose for an adult is 3 
to 4 grams (one gram has been fatal to a child), 
although some people have taken much larger 
doses and survived. 

Symptoms 

Quinine depresses the cell function throughout 
the body, affecting the heart, kidney, liver, and 
central nervous system. Quinine toxicity causes a 
syndrome called cinchonism, which causes tinni- 
tus (ringing in the ears), blurred vision, weakness, 
nausea, vomiting, low blood pressure, and heart 
problems. Evidence of the drug's effect on the brain 
can be seen in the resulting apprehension, confu- 
sion, and excitement. Convulsions and respiratory 
arrest have also been reported, and death occurs 
from respiratory or circulatory collapse in a few 
hours to a few days. 

If the victim recovers, there may be resid- 
ual damage to the eyes and ears — even causing 
deafness. 

Treatment 

There is no antidote to quinine. Perform gastric 
lavage, followed by the administration of magne- 
sium sulfate or activated charcoal. Do not induce 
vomiting. Give hypertonic sodium bicarbonate for 
heart problems. 
See also quinidine. 



radiation poisoning Although excessive exposure 
to radiation is rare, it is a potentially catastrophic 
possibility in the nuclear age. Radiation poisoning 
may occur from internal or external contamination 
and from particle-emitting solids, liquids, or gases 
(including beta and alpha particles, neutrons, pro- 
tons, and positrons) and electromagnetic sources 
(such as X-rays or gamma rays). 

Radiation interferes with the function of the 
body and damages RNA and DNA. Cells that turn 
over quickly, such as those found in the skin or gas- 
trointestinal tract, are affected first. While contact 
with electromagnetic sources of radiation does not 
make the victim radioactive or dangerous to others, 
exposure to particle-emitting sources can be very 
contaminating to anyone who comes in contact 
with the victim. 

Radiation dose is expressed in various terms, but 
rad (radiation absorbed dose) is the most common. 

Symptoms 

Symptoms are dose related: Exposure to 100 to 200 
rads causes nausea, vomiting, abdominal cramps, 
and diarrhea; 200 rads is potentially fatal, and 600 
rads is nearly always fatal within a few days, caus- 
ing severe gastroenteritis and marked dehydration. 
Brief exposure to excessive amounts (5,000 rads 
or more) causes confusion and lethargy followed 
within minutes to hours by convulsions, coma, 
cardiovascular collapse, and death. 

In addition, exposure from anywhere between 
200 and 1,000 rads often depresses the bone mar- 
row function, opening the way to infections. Other 
symptoms include skin burns and hair loss. 

Treatment 

For expert assistance in evaluation and treatment, 
contact the federal Oak Ridge Radiation Emer- 



gency Assistance Center and Training Site (avail- 
able 24 hours a day) at (865) 576-3131. Chelating 
agents may be useful for ingestion or inhalation of 
certain particles. Treat symptoms, maintain airway 
and replace fluid losses. 

For particulate exposure, move the victim from 
the area, remove all clothing, and wash the skin 
with soap and water; all water and clothing must 
be properly destroyed. Rescuers and hospital per- 
sonnel should wear protective gear. Induce vomit- 
ing or perform gastric lavage in cases of ingestion. 

radon This invisible, odorless radioactive gas 
is created by the natural decay of radium and 
uranium found in rocks and soil. It is relatively 
harmless out of doors; it is most dangerous once it 
has seeped inside a house, where it breaks down 
into harmful elements that attach to dust par- 
ticles that can enter the lungs. Once in the lungs, 
the elements decay in minutes, releasing alpha 
radiation. This radiation can cause cell damage 
possibly leading to lung cancer, and is among the 
most dangerous of toxic substances because of the 
number of cases of cancer it is estimated to cause 
each year. 

According to EPA estimates, radon is the number 
one cause of lung cancer among nonsmokers and 
the second leading cause of lung cancer. Experts 
believe radon is responsible for about 21,000 
deaths by lung cancer every year, and that about 
2,900 of these deaths occur among nonsmokers. 

According to the Environmental Protection 
Agency (EPA), it is estimated that one in 1 5 Ameri- 
can homes has levels of radon high enough to pose 
a health risk. And another study of 552 homes sug- 
gested that there are about one milhon homes in 
the United States where the chances of developing 



215 



216 ragwort 



lung cancer from radon are at least as great as one 
in 40 over a lifetime. 

But in a f99f survey by the American Lung 
Association, only 1 1 percent of Americans had 
tested their homes for radon. Further, animal stud- 
ies suggest that in an average home in the United 
States, an individual has about a one in 300 chance 
of developing lung cancer in his or her lifetime 
from indoor radon — or that about 1 0 percent of all 
cases of lung cancer in this country are caused by 
this gas. (It must be remembered, however, that 
smokers are more susceptible to cancer from radon 
than nonsmokers.) 

Radon is able to enter a building because of the 
small difference between inside and outside air pres- 
sure, which draws in the radon in much the same 
way as a fire draws heated air up a chimney: A 
heated house draws cool air from the basement or 
ground floor, where the pressure is low, and sends it 
to the upper floors, where the pressure is higher. 

There are two main types of radon test kits avail- 
able (see Appendix A), and both types are simple, 
inexpensive, and available at local hardware stores. 
Short-term tests remain in your home for two to 
90 days. These tests come in the form of charcoal 
canisters, alpha tracks, electret ion chambers, con- 
tinuous monitors, and charcoal liquid scintillation 
detectors. Because radon levels vary from day to 
day and season to season, short-term tests are less 
likely to give you an accurate picture of your yearly 
exposure. Short-term tests are usually used when 
you need results quickly, such as when you are 
selling your home. 

Long-term tests remain in your home for more 
than 90 days. The most commonly used tests for 
this purpose are alpha track and electret detec- 
tors. The results of long-term tests provide a more 
accurate annual average radon level than a short- 
term test. Because there is no known safe level of 
radon exposure, the EPA recommends that homes 
with radon levels of 2.0 to 4.0 picocuries per liter 
or greater should be remedied. The average radon 
concentration in the indoor air of homes in the 
United States is 1.3 picocuries per liter, while the 
average concentration of radon in outdoor air is 0.4 
picocuries per liter. 

If radon is found in the home, there are several 
options to deal with it. The basement or crawl 



spaces of most houses have a slightly lower air 
pressure than the soil beneath, and this speeds the 
rate at which the gas can enter the house through 
the foundation. One way to cut down on the prob- 
lem is to install pipes to the outdoors that ventilate 
the soil beneath the house. Or, consumers could 
pressurize the basement or crawl space with an air 
blower, flushing out the radon. Sealing cracks in 
the foundation and basement floor has not been 
shown to be an effective way to reduce the inflow 
of radon. 



ragwort (Senecio) [Other names: butterweed, 
squaw weed, stinking willie, tansy ragwort. In the 
United States, groundsel, ragwort, and butterweed 
are commonly applied to many different varieties of 
Senecio.] There are about 3,000 species of Senecio, 
including threadleaf groundsel (S. longilobus) and 
common groundsel (S. vulgaris): many of the variet- 
ies contain poisonous alkaloids. 

Ragwort is a four-foot-tall biennial or perennial 
herb with yellow flower clusters that has become 
naturalized in parts of Canada south to Massachu- 
setts and in Washington and Oregon west of the 
Cascades. 

Threadleaf groundsel is a shrubby perennial 
with white flowers found in Colorado and Utah 
south to western Texas and northern Mexico. 

Common groundsel is a smaller annual with 
soft, fleshy leaves and yellow flowers that has 
become naturalized in Alaska and throughout 
Canada south to North Carolina and west to Wis- 
consin; it is also found in California, New Mexico, 
and Texas. 

Poisonous part 

The entire plant is poisonous; honey made from 
the nectar and milk from animals who have grazed 
on these plants also contain the poisonous pyr- 
rolizidine alkaloids. In general, poisonings have 
occurred from excessive drinking of herbal teas 
made from this plant. Ragwort's toxins can also 
be absorbed through the skin or inhaled as pollen. 
Once inside the body, the poisons damage liver 
cells in a slow and irreversible process that results 
in cirrhosis months or even years later. For grazing 
animals, new research indicates that the seedlings 



rattlesnake, cascabel 217 



may be more toxic than the mature plants. While 
horses and other grazing animals typically avoid 
the mature plant, the seedlings often go undetected 
and are eaten along with grasses. 

Symptoms 

Abdominal pain; anorexia with nausea, vomiting, 
and diarrhea. Chronic use of tea made from these 
plants can result in fatal cases of cirrhosis. 

Treatment 

There is no treatment for this type of liver disease 
caused by the pyrrolizidine alkaloids. 
See also alkaloids. 



rat poison Most rat poisons (or rodenticides) 
that are the most toxic to humans and pets are 
restricted for use only by commercial extermina- 
tors and government agencies. Inorganic rat poison 
compounds include arsenic, thallium, phosphorus, 
barium carbonate, zinc phosphide, and Vacor. 
Organic compounds include sodium fluoroace- 
tate, alphanaphthylthiourea, warfarin, red squill, 
strychnine sulfate, and dicarboximide. 

There are two types of rodenticides: single dose 
(or acute) compounds and chronic varieties, such 
as the anticoagulant rat poisons. Acute poisons kill 
rats after a single feeding and usually include red 
squill, zinc phosphide, strychnine, arsenic, phos- 
phorus, and thallium sulfate. Chronic rat poisons, 
on the other hand, are preferred, since they do 
not produce symptoms in the rat that make it stop 
eating before acquiring a fatal dose, and anticoagu- 
lants are less toxic to humans and animals. 

Poisoning with anticoagulant rodenticides is 
extremely rare, since huge doses would be needed 
in order to be toxic. When it occurs, the treat- 
ment is the administration of vitamin Ki or blood 
transfusions. 

See also arsenic; phosphorus; red squill; thal- 
lium; Vacor; warfarin. 

rattlesnake, canebrake (Crotalus horridus 
atricaudatus) This snake is one of a number of 
species of rattlesnakes known as pit vipers because 
of their heat-sensing pits behind the eyes and nose. 



with tail rattles that hiss before striking. The cane- 
brake is the southern United States' version of the 
timber rattler. 

Symptoms 

Symptoms appear within 15 minutes and include 
excessive thirst, nausea, vomiting, shock, paraly- 
sis, respiratory problems, anemia, necrosis, kidney 
problems, and sometimes death. The bite of a 
rattlesnake is painful. Indications of a serious bite 
include swelling above the elbows or knees within 
two hours, hemorrhages, numbness at the punc- 
ture site, tingling around the mouth, yellow vision, 
vomiting, and violent spasms. 

Treatment 

Antivenin is available. Local care of the bite site is 
essential. Antibiotics and tetanus vaccine should 
be given. 

See also massasauga; pit vipers; rattlesnake, 
cascabel; rattlesnake, eastern diamondback; 
rattlesnake, mexican west coast, rattlesnake, 

RED diamondback; RATTLESNAKE, TIMBER; RATTLE- 
SNAKE, WESTERN diamondback; RATTLESNAKES; SIDE- 
WINDER; SNAKES, POISONOUS; VIPER, GABOON; VIPER, 

jumping; VIPER, Malayan pit; viper, Russel's; viper, 
sawscaled; viper, Wagler's pit; vipers; water 
moccasin; wutu. 

rattlesnake, cascabel (Crotalus durissus) Also 
known as the tropical or South American rattler, 
the cascabel is one of the two most deadly rattle- 
snakes in the world and is found in tropical South 
America. 

Poisonous part 

Crotamine, a toxin that causes convulsions, is 
found in the venom of this snake, which also 
relaxes the victim's neck muscles, causing the head 
to flop and adding to this snake's reputation as a 
neck breaker. 

Symptoms 

Symptoms appear within 15 minutes and include 
excessive thirst, nausea, vomiting, shock, paraly- 
sis, respiratory problems, anemia, necrosis, kidney 
problems, and sometimes death. The bite of a 



218 rattlesnake, eastern diamondback 



rattlesnake is painful. Indications of a serious bite 
include swelling above the elbows or knees within 
two hours, hemorrhages, numbness at the punc- 
ture site, tingling around the mouth, yellow vision, 
vomiting, and violent spasms. 

Treatment 

Antivenin is available. 

See also massasauga; pit vipers; rattlesnake, 
canebrake; rattlesnake, eastern diamondback; 
rattlesnake, mexican west coast; rattlesnake, 
red diamondback; rattlesnake, timber; rattle- 
SNAKE, WESTERN diamondback; RATTLESNAKES; SIDE- 
WINDER; SNAKES, poisonous; VIPER, GABOON; VIPER, 

JUMPING; VIPER, Malayan pit; viper, Russell's; 
VIPER, sawscaled; viper, Wagler's pit; viper, water 
moccasin; wutu. 

rattlesnake, eastern diamondback (Crotalus 
adamanteus) Also called the Florida diamond- 
back, this snake is considered to be the most dan- 
gerous in North America, with a venom highly 
destructive to blood tissue. The largest of all the 
rattlesnakes and heavier than its western relative, 
the eastern diamondback has large dark brown or 
black diamonds with light centers on a body color 
of olive, brown, or black and grows to be eight feet 
long. There are also prominent light diagonal lines 
on the side of its head. It has a heavy body with a 
large, sharply distinct head. 

It is found in sparse woodland, dry pine flat- 
woods, abandoned farms and lowland coastal 
regions of the southeastern Gulf states of the 
United States and throughout Florida. However, 
the population has been reduced by hunters and 
land development. 

Symptoms 

Symptoms appear within 15 minutes and include 
excessive thirst, nausea, vomiting, shock, paraly- 
sis, respiratory problems, anemia, necrosis, kidney 
problems, and sometimes death. The bite of a 
rattlesnake is painful. Indications of a serious bite 
include swelling above the elbows or knees within 
two hours, hemorrhages, numbness at the punc- 
ture site, tingling around the mouth, yellow vision, 
vomiting, and violent spasms. 



Treatment 

Antivenin is available. 

See also massasauga; pit vipers; rattlesnake, 
canebrake; rattlesnake, cascabel; rattlesnake, 
Mexican west coast; rattlesnake, red diamond- 
back; rattlesnake, timber; rattlesnake, western 
diamondback; rattlesnakes; sidewinder; snakes, 

POISONOUS, viper, GABOON; VIPER, JUMPING; VIPER, 

Malayan pit; viper, Russell's; viper, sawscaled; 
VIPER, Wagler's pit; vipers; water moccasin; wutu. 

rattlesnake, horned See sidewinder. 

rattlesnake, Mexican west coast (Crotalus 
basiliscus) The world's second most deadly rattle- 
snake, the Mexican west coast rattlesnake is found 
in western Mexico. 

Symptoms 

Symptoms appear within 15 minutes and include 
excessive thirst, nausea, vomiting, shock, paraly- 
sis, respiratory problems, anemia, necrosis, kidney 
problems, and sometimes death. The bite of a 
rattlesnake is painful. Indications of a serious bite 
include swelling above the elbows or knees within 
two hours, hemorrhages, numbness at the punc- 
ture site, tingling around the mouth, yellow vision, 
vomiting, and violent spasms. 

Treatment 

Antivenin is available. 

See also massasauga; pit vipers; rattlesnake, 
canebrake; rattlesnake, cascabel; rattlesnake, 
eastern diamondback; rattlesnake, red dia- 
mondback; rattlesnake, timber; rattlesnake, 

WESTERN diamondback; RATTLESNAKES; SIDEWINDER; 
SNAKES, poisonous; VIPER, GABOON; VIPER, JUMP- 
ING; VIPER, Malayan pit; viper, Russell's; viper, 
sawscaled; viper, Wagler's pit; vipers; water 
moccasin; wutu. 

rattlesnake, red diamondback (Crotalus ruber) 

This rattler looks very much like the western dia- 
mondback rattlesnake, but its body color is more 
reddish or pinkish and its markings less distinct. 



rattlesnake, western diamondback 219 



It has diamond shapes down its midline, usually 
edged in lighter colors. Black and white rings circle 
the tail. 

This snake prefers arid and semidesert, cold 
coastal regions in the foothills and mountains in 
southern California, Baja California, and northern 
Mexico. It is most often seen during the spring 
sheltering in the sun or crossing the road at night. 

Symptoms 

Symptoms appear within 15 minutes and include 
excessive thirst, nausea, vomiting, shock, paraly- 
sis, respiratory problems, anemia, necrosis, kidney 
problems, and sometimes death. The bite of a 
rattlesnake is painful. Indications of a serious bite 
include swelling above the elbows or knees within 
two hours, hemorrhages, numbness at the punc- 
ture site, tingling around the mouth, yellow vision, 
vomiting, and violent spasms. 

Treatment 

Antivenin is available. 

See also massasauga; pit vipers; rattlesnake, 
canebrake; rattlesnake, cascabel; rattlesnake, 

EASTERN diamondback; RATTLESNAKE, MEXICAN 
WEST coast; rattlesnake, TIMBER; RATTLESNAKE, 
WESTERN diamondback; RATTLESNAKES; SIDEWINDER; 
SNAKES, POISONOUS; VIPER, GABOON; VIPER, JUMP- 
ING; VIPER, Malayan pit; viper, Russell's; viper, 
sawscaled; viper, Wagler's pit; vipers; water 
moccasin; wutu. 

rattlesnake, South American See rattlesnake, 
cascabel. 

rattlesnake, timber (Crotalus horridus) The only 
rattler found in the populated northeastern United 
States, the timber rattlesnake has a range extend- 
ing into much of the central and southern states 
except for Florida. As a result of urban pressure, 
this species has been exterminated in many parts 
of its range. 

There are two distinct races of the timber rattler: 
C. h. horridus, found in the northern part of the spe- 
cies' range in pine forests and wooded slopes; and 
the canebrake rattlesnake, C. h. atricaudatus, found 



in southern lowlands in cane thickets and swamps. 
The timber rattler is large, with a robust body and a 
large, flat unmarked head. Its color is yellow brown 
or dark brown, with darker crossbands; completely 
black snakes are not uncommon. The canebrake 
rattler is more brightly marked, with a pink buff 
or brown color with bold black crossbands and 
an orange or red dorsal stripe. Both types have a 
black tail. 

The timber rattler is often seen coiled up and 
motionless waiting for prey in the daytime dur- 
ing spring and fall, and on summer nights. In the 
north, large groups of timber rattlers can be seen in 
rocky dens, sometimes with copperheads. 

Symptoms 

Symptoms appear within 15 minutes and include 
excessive thirst, nausea, vomiting, shock, paraly- 
sis, respiratory problems, anemia, necrosis, kidney 
problems, and sometimes death. The bite of a 
rattlesnake is painful. Indications of a serious bite 
include swelling above the elbows or knees within 
two hours, hemorrhages, numbness at the punc- 
ture site, tingling around the mouth, yellow vision, 
vomiting, and violent spasms. 

Treatment 

Antivenin is available. 

See also massasauga; rattlesnake, canebrake; 
rattlesnake, cascabel; rattlesnake, eastern dia- 
mondback; rattlesnake, Mexican west coast; 
rattlesnake, red diamondback; rattlesnakes. 



rattlesnake, tropical See rattlesnake, cascabel. 



rattlesnake, western diamondback (Crotalus 
atrox) Also called a coon tail rattler, this is the 
largest rattlesnake of the North American West. 
The western diamondback has a heavy body, with 
a large, spade-shaped head that is distinct from the 
neck. The body color is gray-brown or pink, with 
light-bordered, dark diamond blotches on the back. 
The diamonds are often covered with small dark 
spots, which are often faded and dusty looking. 
The tail is distinctive, ringed boldly with black and 



220 rattlesnakes 



white. There are two light diagonal lines on the 
side of its face, and the stripe behind the eye meets 
the upper lip in front of the jaw angle. 

The western diamondback is found in the 
semidesert and dry arid areas, rocky canyons, 
river bluffs, and some cultivated areas in much of 
the southwestern parts of the United States from 
southeastern California east to central Arkansas, 
and as far south as central Mexico. Toxicologists 
consider this snake to be the most dangerous snake 
in the United States. 

When threatened, the western diamondback 
stands its ground, lifts up its head and sounds a 
"rattling" warning. It is most active late in the day 
during the hot summer months. 

Symptoms 

Symptoms appear within 15 minutes and include 
excessive thirst, nausea, vomiting, shock, paraly- 
sis, respiratory problems, anemia, necrosis, kidney 
problems, and sometimes death. The bite of a 
rattlesnake is painful. Indications of a serious bite 
include swelling above the elbows or knees within 
two hours, hemorrhages, numbness at the punc- 
ture site, tingling around the mouth, yellow vision, 
vomiting, and violent spasms. 

Treatment 

Antivenin is available. 

See also massasauga; pit vipers; rattlesnake, 
canebrake; rattlesnake, cascabel; rattlesnake, 

EASTERN diamondback; RATTLESNAKE, MEXICAN 
WEST coast; RATTLESNAKE, RED DIAMONDBACK; RAT- 
TLESNAKE, timber; rattlesnakes; sidewinder; viper, 
gaboon; viper, jumping; viper, malayan pit; viper, 
Russell's; viper, Wagler's pit; vipers; water moc- 
casin; WUTU. 

rattlesnakes Rattlesnakes resemble any other 
viper except that they almost all have a rattle at 
the end of the tail formed by a series of dry, horny 
segments that vibrate with a rattling sound when 
shaken by the snake as a warning of its presence. 
Each time the snake loses its skin, a new segment 
is added to the rattle. More than 98 percent of the 
snakebites in the United States are from rattle- 
snakes, which are found in two separate snake 



families: the Crotalidae (the eastern and western 
diamondbacks, the timber rattler, the canebrake 
rattler, the pacific rattler, and the mojave rattler), 
and the Viperidae (the sidewinder, or horned, 
rattler, and two types of pygmy rattlers — the mas- 
sasauga and the pygmy). They are all considered 
pit vipers because of the heat-sensing pits between 
each nostril and eye. 

Outside the United States, the cascabel rattler 
(also known as the tropical or South American rat- 
tler) is found in tropical South America and is one 
of the two most dangerous rattlers. The Mexican 
west coast rattler is the second most dangerous rat- 
tler and is found in western Mexico. The Brazilian 
rattler is found in southeastern Brazil, Argentina, 
and Paraguay. 

Although rattlesnake are poisonous, fatalities in 
the United States are rare because antivenin is usu- 
ally available immediately. 

Poisonous part 

Rattlesnake venom includes the toxin acetylcholin- 
esterase, and in some tropical varieties the convul- 
sion-inducing toxin crotamine also appears. 

Symptoms 

Within 15 minutes to an hour after being bitten, 
the victim will begin to experience thirst, nausea, 
vomiting, paralysis, shock, respiratory distress, and 
drooping eyelids. Death follows malfunction of the 
kidneys. Tinghng around the mouth, yellow vision, 
and a numbed wound site all are indicative of a 
serious bite with a large amount of venom. In cases 
of severe poisoning, there will be swelling caused 
by hemorrhages above the elbows or knees within 
two hours. 

Treatment 

Antivenin is available. 

See also massasauga; pit vipers; rattlesnake, 
canebrake; rattlesnake, cascabel; rattlesnake, 

EASTERN diamondback; RATTLESNAKE, MEXICAN 
WEST coast; RATTLESNAKE, RED DIAMONDBACK; 
RATTLESNAKE, TIMBER; RATTLESNAKE, WESTERN DIA- 
MONDBACK; sidewtnder; snakes, poisonous; viper, 

GABOON; viper, JUMPING; VIPER, MALAYAN PIT; VIPER, 

Russell's; viper, sawscaled; viper, Wagler's pit; 
vipers; water moccasin; wutu. 



rhubarb 221 



red squill This botanic rat poison is one of the 
least toxic of all the organic rodenticides available. 
When ingested in large doses, it can interfere with 
the function of the heart; it is also an irritant and 
central-acting emetic. 

Symptoms 

Acute poisoning causes nausea, vomiting, diarrhea, 
abdominal pain, cardiac irregularities, convulsion, 
and death from ventricular fibrillation. 

Treatment 

Induce vomiting with syrup of ipecac followed by 
gastric lavage. Administer lidocaine or phenytoin; 
monitor electrolytes. 
See also rat poison. 

rescue, procedures for smoke and fumes Poi- 
soning by smoke, gas, or chemical fumes requires 
special rescue methods. It is CRITICALLY IMPOR- 
TANT that you do not light a match, turn on a light 
switch, or produce a flame or spark in the presence 
of gas or fumes. 

If you are alone, call for help before attempting 
to rescue the victim. To avoid poisoning yourself, 
hold your breath. Before you enter the affected 
area, take several breaths of fresh air, then inhale 
deeply as you go in. If smoke and fumes are visible 
in the upper part of the room, stay below them by 
crawling. If auto exhaust or other heavy fumes are 
visible near the floor, keep your head above them. 
Remove the victim immediately. Do not perform 
first aid until you reach fresh air. 

resins Also called resinoids, these compounds are 
made up of a wide variety of substances that are 
both resinous and semisolid at room temperature, 
and include potent toxins such as those found 
in rhododendron and laurel. Symptoms of resin 
poisoning include stomach irritation, vomiting, 
diarrhea, headache, weakness, irregular heartbeat, 
convulsions, coma, and, sometimes, death. 
See also laurel, mountain; rhododendron. 

rhododendron (Rhododendron) Once considered 
as belonging to two separate genera, rhododendron 



and azalea are now both considered to be in the Rho- 
dodendron genus. There are about 800 Rhododendron 
species, which are subdivided into eight subgenera. 

This extremely common evergreen, semiever- 
green, and deciduous shrub is found everywhere 
throughout Canada, Britain, and the United States 
(except for the north central states and subtropical 
Florida). Rhododendrons are odorless, with bell- 
shaped flowers that come in a variety of colors; 
azaleas are sweet smelhng with funnel-shaped 
flowers. Both are deadly narcotics said to have 
poisoned Xenophon's army from honey made from 
the flowers' nectar. 

Poisonous part 

All parts of the plant are poisonous and contain 
carbohydrate andromedotoxin — the same poison 
found in mountain laurel. Honey made from the 
plant's nectar has also caused poisoning. Children 
who have chewed on the leaves have become seri- 
ously poisoned. 

Symptoms 

Burning in the mouth, followed within six hours of 
ingestion by increased salivation, vomiting, tearing 
eyes, nasal discharge, prickling skin, difficulty in 
breathing, slow heartbeat, muscle weakness pro- 
gressing to paralysis, convulsions, coma, and death. 

Treatment 

Fluids and electrolyte replacement; atropine for 
slow heart rate; ephedrine for low blood pressure. 
See also laurel, mountain. 



rhubarb (Rheum rhabarbarum; sometimes incor- 
rectly referred to as R. rhaponticum) [Other names: 
pie plant, wine plant.] This common perennial, 
grown for its tasty stalk, has poisonous leaves that 
can be fatal if mistakenly cooked along with the 
rhubarb stalks or eaten raw. 

Several feet tall at maturity, the plant has large, 
wavy oval leaves and is cultivated across the United 
States for its edible stalk. 

Poisonous part 

The leaves are the only poisonous part of the rhu- 
barb plant and contain oxalic acid, potassium and 



222 ringhals 



calcium oxalates, and anthraquinone glycosides. 
They must be removed before eating or cooking. 

Symptoms 

Several hours after ingestion, the digestive irritant 
in the leaves can cause stomach pain, nausea, vom- 
iting, hemorrhage, respiratory problems, burning 
mouth, and possibly cardiac or respiratory arrest 
following a drop in the calcium content of the 
blood. Without treatment, death or permanent 
kidney damage may occur. It is believed that symp- 
toms are almost completely caused by the anthra- 
quinone cathartics in the leaves. 

Treatment 

Gastric lavage, together with calcium salts, calcium 
gluconate, and other forms, helps remove the 
oxalate. Fluids must be replaced to prevent kidney 
malfunction. 

See also oxalates. 

ringhals (Hemachatus hemachatus) One of the 

spitting cobras, this brick-red snake is found in South 
Africa and prefers to spray venom toward the eyes 
rather than bite. The openings of the venom ducts 
are on the front of its fangs, so that when faced with 
an enemy the ringhals can apply muscular pressure 
on the gland to force the liquid in a stream straight 
at the enemy's eyes. The aim of the ringhals is abso- 
lutely deadly, and they are a real threat because they 
have a range of up to 10 feet. Spitting cobras can 
also bite, but they seem reluctant to do so. 

Symptoms 

When contact is made with the eyes, there is 
excruciating pain and sometimes permanent blind- 
ness; there is also weakness, respiratory distress, 
collapse, and death. 

Treatment 

Antivenin is available, but only the specific antise- 
rum for the type of cobra involved should be used, 
and victims are often tested for sensitivity before 
being treated. If the eyes are contaminated, they 
should be immediately flushed out and treated or 
blindness may result. 

See also cobra; cobra, spitting; snakes, 

POISONOUS. 



Ritalin Known chemically as methylphenidate, 
this drug is a stimulant but is ironically given to 
hyperactive children to calm them down. In adults, 
it acts as a central nervous system stimulant and, if 
taken with monoamine oxidase (MAO) inhibitors, 
can drastically increase blood pressure. It is well 
absorbed when taken by mouth and is metabolized 
extensively by the liver. It has a low therapeutic 
index (that is, toxicity occurs at levels only slightly 
above the usual doses). A high degree of tolerance 
can occur after continued use. 

Symptoms 

Overdose can cause agitation, nausea, vomiting, 
hyperthermia, tremors, seizures, hypertension, 
coma, and convulsions; if taken with anticonvul- 
sants, it may change seizure pattern. An overdose 
can be fatal. 

Treatment 

Treat symptoms if they occur. There is no specific 
antidote for Ritalin; hypertension may be treated 
with a vasodilator such as phentolamine. Do 
not induce vomiting; perform gastric lavage and 
administer activated charcoal. 



rosary pea (Abrus precatorius) [Other names: bead 
vine, black-eyed Susan, coral bead plant, crab's 
eyes, Indian licorice, jequirity bean, licorice vine, 
love bean, lucky bean, mienie-mienie Indian bean, 
paternoster pea, prayer bead, precatory bean, red 
bead vine, rosary bean, Seminole bead, weather 
plant, wild licorice.] This climbing, woody vine is 
found in tropical regions in Africa and Asia, and in 
Florida, Hawaii, Guam, Central America, southern 
Europe, and India. Its leaves have short leaflets 
that droop at night and in cloudy weather, and its 
pea-shaped fruit pod holds five scarlet, pea-sized 
seeds with hard seed coats and a small black spot. 
Its seeds are used in rosaries, bracelets, leis, good 
luck charms, and children's toys, but the seeds are 
harmless unless chewed. 

Poisonous part 

Seeds, or beans, if chewed. If swallowed whole, 
the hard seed coat prevents absorption and poison- 
ing. The toxalbumin called abrin, one of nature's 



rust remover 223 



most poisonous substances, is the poison in rosary 
pea; the tetanic glycoside abric acid is found in the 
seeds. Abrin interferes with the protein synthesis in 
cells of the intestinal wall. 

Symptoms 

The severity of symptoms, which appear from sev- 
eral hours to several days after eating, depends on 
the number of beans eaten and how much they 
were chewed. Symptoms include mouth irritations, 
nausea, vomiting, severe diarrhea, acute gastroen- 
teritis, chills, weakness, clammy skin with perspi- 
ration, weak, rapid pulse, and convulsions ending 
in death from heart failure. One seed chewed by a 
child can be fatal despite intensive care. 

Treatment 

The long time between ingestion and symptoms 
allows for the removal of the poisonous substance; 
convulsions are treated as they occur, together with 
a high carbohydrate diet to head off liver damage. 
See also glycoside; phytotoxins. 

roseum A variety of chrysanthemum used in the 
production of the botanic insecticide pyrethrum. 
See also pyrethrum. 



rotenone Also known as derrin or derris, rotenone 
is a broad-spectrum botanic insecticide derived from 
the derris root and used in lotions and ointments 



to treat chiggers, scabies, and head lice; in dusts, 
washes, and dips against animal parasites; and in 
insecticide sprays for home and agricultural use. 
Once believed to be harmless, it is now known to be 
more toxic than pyrethrin. While it has been used 
for many years, it has regained popularity in the last 
decade because it kills a wide variety of insects and 
is easy to make. This white, odorless crystal is sold 
in a 1 percent and 5 percent powder or spray. 

Symptoms 

Rotenone affects the nervous system and is most 
toxic when inhaled; skin contamination can cause 
a local irritation, and ingestion will cause stomach 
irritations but it is rarely fatal. If inhaled, it can 
cause vomiting, abdominal pain, tremors, and 
incoordination and can lead to convulsions and 
death from respiratory failure. Skin contact causes 
local irritation and dermatitis; ingestion produces 
nausea and vomiting. Chronic poisoning can cause 
kidney and liver damage. 

Treatment 

Symptomatic. 

See also botanic insecticides; derris; 
pyrethrin. 



rubbing alcohol See isopropyl alcohol. 
rust remover See alkaline corrosives. 



s 



saccharin Saccharin is an artificial sweetener 
discovered by accident in 1878 that is 400 times 
as sweet as sugar; American consumers ate or 
drank more than 5 million pounds of it a year 
before it was banned. Although the Food and 
Drug Administration banned saccharin in March 
1977 because it is mutagenic and causes cancer 
in laboratory animals, it is still an ingredient in 
many low-calorie and sugar-free foods, includ- 
ing soft drinks, baked goods, jams, canned fruit, 
candy, dessert toppings, and salad dressings, and 
in almost all toothpastes in the United States. It 
is also the major ingredient in Sweet'n Low, the 
sweetener in the pink packets, which (like all 
foods that contain saccharin) carries a mandatory 
warning label that might be removed should sac- 
charin ever lose its classification as a suspected 
carcinogen. 

A Canadian scientist first identified it as a pos- 
sible carcinogen in 1977 and the FDA proposed a 
ban. But the public was outraged at the FDA's plan, 
since another artificial sweetener (cyclamate) had 
already been taken off the market after studies had 
cited it as a cause of cancer. Diabetics, who rely 
on artificial sweeteners, argued that they needed 
saccharin. 

In a compromise. Congress passed a law pre- 
venting the ban but requiring the warning labels. 
In 1981, saccharin went on the government's 
list, which now has 169 suspected carcinogens 
and 29 known carcinogens. Its name is derived 
from the Latin word saccharun, meaning "sugar"; 
pure saccharin is an odorless white powder that 
easily dissolves in warm water but is destroyed 
by high heat. It has been criticized almost from 
the beginning of its use, first because it offered 
no food value and later because of its animal 
carcinogenicity. 



Symptoms 

Ingestion of large amounts can produce toxic 
symptoms such as vomiting, diarrhea, abdominal 
pain, frothing, muscle spasms, convulsions, and 
stupor. In hypersensitive persons, even small doses 
may cause gastrointestinal symptoms such as vom- 
iting and diarrhea, and allergic skin reactions. 

Treatment 

Gastric lavage or induced vomiting for large over- 
doses, followed by a saline cathartic; symptomatic 
treatment. 

See also sweeteners, artificial. 

salicylates Widely valued for their painkilling 
and anti-inflammatory properties, the salicylates 
are found in a wide variety of over-the-counter 
preparations and cold products. The substance is 
an ingredient in aspirin and in most other analgesic 
preparations, and before the introduction of child- 
resistant caps, salicylate poisoning was one of the 
leading causes of accidental death in children. Oil 
of wintergreen, found in many skin ointments, is 
also high in salicylate content and can be fatal if 
ingested. 

Aspirin should never be taken with acetamino- 
phen (Tylenol), since it increases the liver toxicity 
of the Tylenol. Aspirin also increases the activity of 
blood thinners. Vitamin C in large doses taken with 
aspirin can cause poisoning, but this is not usually 
fatal. Aspirin also interferes with the utilization of 
vitamin K in the liver. 

Symptoms 

Salicylate poisoning causes a wide range of symp- 
toms depending on the person's age and the 
amount swallowed. Two distinct syndromes may 



224 



salmonellosis 225 



occur depending on whether the exposure is 
chronic or acute: acute ingestion of 1 50 to 200 mil- 
ligrams per kilogram will produce a mild reaction; 
ingestion of 300 to 500 milligrams per kilogram 
will produce a more serious response. Chronic 
intoxication may occur with ingestion of 100 mil- 
ligrams per kilogram for two or more days. 

Onset of symptoms may be delayed for 12 to 
24 hours. In cases of acute poisoning, vomiting 
is followed by ringing in the ears and lethargy; 
severe poisoning causes coma, seizures, low blood 
sugar, high fever, and pulmonary edema followed 
by death due to central nervous system failure and 
cardiovascular collapse. 

Chronic poisoning may result with older per- 
sons who have become confused over their dosage, 
or with young children. Symptoms include confu- 
sion, dehydration, and acidosis, which may often 
be misdiagnosed. With chronic poisoning, death 
rates are much higher and cerebral and pulmonary 
edema are more common. 

Treatment 

There is no specific antidote for salicylate poison- 
ing, but sodium bicarbonate is often given to help 
the kidneys eliminate the drug. Treat symptoms, 
replace fluid, and maintain electrolyte balance; 
induce vomiting or perform gastric lavage followed 
by the administration of activated charcoal and a 
cathartic. With very large ingestions of salicylate, 
very large doses of activated charcoal are also 
needed to absorb the salicylate. Hemodialysis can be 
effective in removing salicylate. The victim should 
be treated for shock until medical care is available. 
See also aspirin. 

Salmonella Bacteria (including S. enteritidis, S. 
cubana, S. aertrycke, S. choleraesius) that multiply 
rapidly at room temperature and cause salmonel- 
losis, an illness characterized by nausea, vomiting, 
and diarrhea. Salmonella is found in raw meats, 
poultry, eggs, fish, raw milk, and foods made from 
them, as well as in pet turtles and marijuana. 
See also salmonellosis. 

salmonellosis One of the most common types 
of food poisoning, typically associated with a very 



wide range of foods. It is caused by one of the more 
than 2,300 strains of Salmonella that multiply rap- 
idly at room temperatures; Salmonella enteritidis and 
S. typhimurium are the most common. According to 
the FDA Bad Bug Book, 2 million to 4 million cases of 
salmonellosis occur in the United States each year, 
yet only about 40,000 cases are reported, as many 
mild cases are not diagnosed or reported. An esti- 
mated 1,000 people die of the condition each year. 

Salmonellosis occurs in raw or undercooked 
poultry and eggs, raw meats, fish, nonpasteur- 
ized milk, and any foods made from them. Most 
recently, a large outbreak (more than 1,300 people 
affected as of August 2008) that covered 43 states 
involved jalapeno and Serrano peppers imported 
from Mexico. Originally this outbreak, which was 
caused by a rare strain of Salmonella called S. saint- 
paul, was attributed to tomatoes, and tomato sales 
slumped dramatically. However, further investiga- 
tion by the Food and Drug Administration and 
others uncovered the pepper connection and dis- 
missed the case against the tomatoes. An outbreak 
of salmonellosis in Oregon in March 2008 involved 
cantaloupe, while another in 2002 affected 650 
people from all 50 states and was linked to a Dallas 
hotel food worker who contaminated the salsa the 
hotel served. 

Symptoms 

From six to 48 hours after eating contaminated 
food, symptoms appear, including severe head- 
ache, nausea, fever, stomach cramps, diarrhea, 
vomiting, and sometimes a rash. Symptoms usu- 
ally last two to seven days, and the infection may 
be mild to severe. It can be fatal, especially in very 
young or very old patients, or those with underly- 
ing impaired immune systems. 

Treatment 

Treatment is symptomatic, including a bland diet 
(liquids and soft solids) and fluids to offset dehy- 
dration. Antibiotic treatment (chloramphenicol, 
ampicillin, or a tetracycline) should be adminis- 
tered only in cases of severe infection, or for people 
at high risk for complications. 

Complications 

Meningitis, blood poisoning, bone/joint infections. 



226 saponin 



Prevention 

Cooks should be sure to prepare and cook chicken, 
eggs, and other poultry and meats completely, and 
to promptly refrigerate leftovers. Consumers also 
should refrigerate eggs and not use them raw 
(such as in eggnog). Raw chicken should never 
touch any other food or utensils during prepara- 
tion, and cooks should wash their hands after 
touching it. 

saponin One of the toxic glycoside compounds 
that vary in strength in any particular plant 
depending on the plant part and time of the 
year. While saponins are not easily absorbed by 
a healthy digestive tract, in the presence of other 
substances irritating to the digestive tract they can 
be absorbed, causing pain, vomiting, and diarrhea 
similar to gastroenteritis. There is still much to 
be learned about the saponins, and many of the 
plants whose toxicity is a result of this compound 
have not been extensively studied. The saponin 
content of any one plant changes according to 
the part of the plant, its stage of growth, and the 
season. 

Plants that contain saponins include the 
corn cockle, tung tree, beech, English ivy, and 
pokeweed. 

See also corn cockle; glycoside; ivy; pokeweed. 

savin (Juniperus sabina) This extremely common 
shrub is found throughout the world and is an 
ancient abortifacient (abortion-inducer); oil made 
from the shrub is used to counteract overdose of 
cardiac medications like digitalis. 

Poisonous part 

The entire savin plant is toxic. 

Symptoms 

In small doses, ingestion causes water loss and starts 
menstruation; in large doses, it causes gastroenteri- 
tis with hemorrhages, vomiting, polyuria (excessive 
urine), oliguria (reduced urine) and anuria (absence 
of urine), and convulsions. Topically, savin oil cause 
blisters. Death from respiratory arrest occurs from 
10 hours to several days later. 



Treatment 

Castor oil followed by gastric lavage or emesis; 
follow immediately with a saline cathartic. Treat 
symptoms; give milk and plenty of fluids. 

saxitoxin A deadly neurotoxin that is produced 
by plankton and causes paralytic shellfish poison- 
ing (PSP). This poison gets its name from the Alas- 
kan butter clam (Saxidomus giganteus), from which 
it is extracted; it blocks nerve impulses, causes 
paralysis of the respiratory muscles and can be 
fatal if even one contaminated shellfish is eaten. It 
has minimal effects on the cardiovascular system. 
Although there is no antidote to saxitoxin, it is 
readily absorbed by activated charcoal. 

See also dinoflagellate; paralytic shellfish 

POISONING; SHELLFISH POISONING. 

scombroid poisoning A type of poisoning caused 
by eating any of a group of scombroid fish (includ- 
ing mackerel, swordfish, moray eel, mahimahi, 
tuna, bluefish) that have begun to spoil when his- 
tamine in the flesh interacts with certain types of 
bacteria. When these fish are allowed to stand at 
room temperature for several hours, the bacteria 
produce a histaminelike substance called saurine. 

Scombroid fish are more susceptible to the 
development of saurine than are most other kinds 
of fish; all of the species that are potentially toxic 
live in temperate or tropical waters (especially 
around Cahfornia and Hawaii). Even commercially 
canned tuna can become toxic, although the most 
common fish responsible is mahimahi. 

In annual reports, scombroid poisonings still 
rank among the top four most often reported 
seafood food poisonings. No doubt consumer mis- 
handling in recreational and home settings can 
contribute to the incidence, and food service estab- 
lishments must be better advised in product selec- 
tion and handling. 

Studies have shown that toxic histamine lev- 
els can be generated within less than six to 12 
hours exposure without ice or refrigeration. This 
problem is of particular concern immediately after 
catch aboard a commercial or recreational boat. 
Likewise, the recreational catch lying on a warm 



scorpion 227 



dock or beach is prone to histamine production in 
certain species. 

Symptoms 

Symptoms of saurine poisoning resemble those of a 
severe allergy: Soon after eating, the victim begins 
to experience headache, throbbing blood vessels 
in the neck, nausea and vomiting, burning throat, 
and massive welts and itching. Recovery begins 
between eight and 12 hours later. 

Treatment 

Antihistamines are usually prescribed. 

Prevention 

The potential toxins are not destroyed by freezing, 
cooking, smoking, curing, or canning. Chemical 
testing is the only reliable way to evaluate a poten- 
tially contaminated product. 

scorpion Looking like a little crab with eight legs 
(in fact, scorpions are cousins to the sea-dwelhng 
crustaceans), the scorpion has a segmented tail that 
curls over the body and ends in a poison reservoir 
and stinger. This tail is so flexible that it is almost 
impossible to pick up a scorpion with the bare 
hands and avoid a sting. The scorpion of the South- 
west inflicts severe pain with its neurotoxic venom 
and is especially dangerous to children. 

Because of its eight legs, it belong to the Arach- 
nida family (as do tarantulas and spiders). Most of 
the more than 700 species are about 3 inches long, 
are either black or yellow and are found in most 
warm regions of the world. 

Some of the most poisonous species are found 
in Mexico, North Africa, South America, parts of 
the Caribbean, and India. About 40 species live in 
the United States, and though the stings of most 
scorpions are more or less harmless, the venom 
of one found in the southern states — the sculp- 
turatus scorpion (Centruroides exilicauda) — contains 
a neurotoxin and can be lethal. Other poisonous 
scorpions in the United States include the brown 
scorpion (C. gertschii) and the common striped scor- 
pion (C. vittatus). 

Poisonous scorpions in Mexico and Brazil are 
the Tityus bahiensis and T. serrulatus; the most deadly 



scorpions in North Africa, India, and Pakistan are 
Androctonus asutralis and Buthus occitanus. 

While scorpions don't attack humans, they hke 
dark, moist places and hide in clothing or shoes, 
where they will sting if stepped on. Because of 
their fondness for the dark and the wet, they often 
crawl into shoes at night, where they present a 
dangerous hazard. In areas with heavy infestations 
of scorpions, residents spread out a wet burlap sack 
at night; scorpions crawl in and can then be easily 
located and destroyed in the morning. 

Poisonous part 

In equal amounts, scorpion venom is proportion- 
ately more poisonous than snake venom; however, 
scorpions inject a smaller amount of venom when 
they sting. The pale yellow desert scorpion is about 
2 inches long and is more lethal than the big black 
scorpion, and the red scorpions are not deadly. The 
poison of the scorpion carries a neurotoxin that 
destroys nerve tissue and disturbs the heart. 

Symptoms 

The first symptom is a severe, sharp, and burn- 
ing pain, similar to a bee sting. If the sting was 
of a nonlethal scorpion, the area of the sting will 
become swollen and discolored and may form a 
blister; symptoms will last for eight to 12 hours. If 
the sting was of the lethal species, the sharp pain 
produced by the sting is quickly followed by a pins- 
and-needles sensation at the sting site. The area of 
the sting will not become swollen or discolored; 
within one to three hours the following symptoms 
will appear: itchy eyes, nose, and throat; tightness 
of jaw muscles and difficulty in speaking; extreme 
restlessness and muscle twitching; muscle spasms 
with pain; nausea, vomiting, and incontinence 
(caused by stimulation of the autonomic nervous 
system); drowsiness, difficulty in breathing, and 
irregular heartbeat. 

Because scorpion toxicity is dose related, fatali- 
ties are uncommon in adults; the smaller the vic- 
tim, the greater the danger of death. Therefore, 
children and the elderly are at higher risk. Symp- 
toms appearing within two to four hours after a 
lethal scorpion sting indicate a serious medical 
problem. Fatalities have occurred as much as four 
days after a scorpion sting. However, it is not true 



228 scorpion, brown 



that any scorpion sting brings death, since very 
few species are toxic enough to be fatal. Only one 
out of a thousand stings is fatal. Interference with 
the absorption of venom will head off serious 
symptoms. 

Treatment 

Contact medical help immediately whether or not 
it is a lethal scorpion sting. Have the person lie still, 
with the bitten part immobile and lower than the 
heart. Apply ice packs to the wound, and apply 
a constricting band two to four inches above the 
bite, snug but loose enough to allow a pulse far- 
ther out on the limb. If swelling reaches the band, 
tie another band two to four inches higher up, 
and then remove tthe first one. After 30 minutes, 
remove the band. If pain is the only symptom, 
a cold compress and painkillers may be enough. 
More severe cases call for local anesthetics and 
powerful painkillers, plus an antivenin to deacti- 
vate the venom. Antivenins against the venoms 
of local, deadly species of scorpion are available in 
most parts of the world where the creatures are 
found. Not recommended: hot packs, alcohol, mor- 
phine, or incisions. 

See also scorpion, brown; scorpion, common 
striped; scorpion, sculpturatus. 

scorpion, brown (Centruroides gertschii) One of 

three species of poisonous scorpions in the United 
States, the brown scorpion lives primarily in the 
Southwest — especially in Arizona. 

Poisonous part 

The sting of the brown scorpion carries a deadly 
neurotoxin far more lethal than snake venom, 
which can destroy nerve tissue and cause heart 
problems. 

Symptoms 

Intense pain, numbness, and hemorrhage of the 
intestines and stomach; lung and seizure activi- 
ties. There is generally only a mild tingling at the 
wound site, followed by throat spasms, restless- 
ness, muscular spasms, stomach cramps, convul- 
sions, blood pressure abnormalities, pulmonary 
edema, and respiratory failure. Symptoms usually 



begin in one to two days, but death can come as 
much as four days after a sting. Still, only one of a 
thousand stings is fatal. 

Treatment 

Antivenin is available. 
See also scorpion. 

scorpion, common striped (Centruroides vittatus) 

One of three poisonous scorpions living in the 
United States, the common striped scorpion lives 
primarily in Arizona and other areas of the Ameri- 
can Southwest. Scorpions live near homes and hke 
the dark warmth of shoes and closets; they are 
not aggressive toward humans unless suddenly 
disturbed. When attacking, the scorpion's front 
pincers grab on and its tail flings forward to sting 
(once or repeatedly). 

Poisonous part 

The sting of the common striped scorpion carries 
a deadly neurotoxin far more lethal than snake 
venom, which can destroy nerve tissue and cause 
heart problems. 

Symptoms 

Intense pain, numbness, and hemorrhage of the 
intestines and stomach; lung and seizure activi- 
ties. There is generally only a mild tingling at the 
wound site, followed by throat spasms, restless- 
ness, muscular spasms, stomach cramps, convul- 
sions, blood pressure abnormalities, pulmonary 
edema, and respiratory failure. Symptoms usually 
begin in one to two days, but death can come as 
much as four days after a sting. Still, only one of a 
thousand stings is fatal. 

Treatment 

Antivenin is available. 
See also scorpion. 

scorpion, sculpturatus (Centruroides exilicauda) 

One of three poisonous scorpions found in Ari- 
zona, New Mexico, and parts of California. The bite 
from the sculpturatus scorpion contains a powerful 
neurotoxin that can be lethal. Scorpions live near 



scorpion fish 229 



homes and like the dark warmth of shoes and clos- 
ets; they are not aggressive toward humans unless 
suddenly disturbed. When attacking, the scorpion's 
front pincers grab on and its tail flings forward to 
sting (once or repeatedly). 

Poisonous part 

The sting of the sculpturatus scorpion carries a 
deadly neurotoxin far more lethal than snake 
venom, which can destroy nerve tissue and cause 
heart problems. 

Symptoms 

Intense pain, numbness, and hemorrhage of the 
intestines and stomach; lung and seizure activi- 
ties. There is generally only a mild tingling at the 
wound site, followed by throat spasms, restless- 
ness, muscular spasms, stomach cramps, convul- 
sions, blood pressure abnormalities, pulmonary 
edema, and respiratory failure. Symptoms usually 
begin in one to two days, but death can come as 
much as four days after a sting. Still, only one of a 
thousand stings is fatal. 

Treatment 

Antivenin is available. 
See also scorpion. 

scorpion fish The family of scorpion fish includes 
about 350 species, some of them as venomous as 
a cobra, that are found in oceans throughout the 
world. The scorpion fish proper is closely related 
to other poisonous members of the Scorpaenidae 
family, including the zebra fish, waspfish, butterfly 
fish, rockfish, stonefish, and lionfish. 

The scorpion fish is found in the reefs and coral 
caves of the Pacific Ocean and is about four to eight 
inches long with a large head and big mouth, col- 
ored in red-brown and white bands. Scorpion fish 
look so much like stones that they can be almost 
unnoticeable and can be easily stepped on when a 
person walks in shallow water. Most scorpion fish 
stings, however, are reported after handling of the 
fish when taking them off the hook or out of a net; 
there are about 300 cases of scorpion fish poisoning 
reported yearly in the United States. Depending on 
the species, scorpion fish have 17 or 18 venomous 



spines that are covered by a layer of skin called 
the integumentary sheath. As each spine enters a 
person's skin, its sheath is pushed down, releasing 
the venom from a gland that lies hidden beneath 
it. This venom is the deadliest poison of any fish, 
lethal enough to kill a swimmer or beachcomber 
in two hours. 

There are about 60 species of rockfish in the scor- 
pion fish family, mostly found in the cool waters of 
the Pacific Ocean. Rockfish have a hard protective 
covering around their heads, as well as the needle- 
sharp spines common to all scorpion fish. 

The most exotic of all the scorpion fish are the 
zebra fish, which usually swim in pairs in the open, 
marked with a striking pattern of stripes and feath- 
ery fins. Among those fins are 18 long, slender, 
pointed spines that deliver a venom that can cause 
a painful and swollen wound leading to gangrene, 
delirium, convulsions, cardiac failure, and even 
death. The zebra fish is found in the Red Sea and 
the Indian Ocean, and in the waters surrounding 
China, Japan, and Australia. Swimmers in these 
areas should avoid approaching a zebra fish, espe- 
cially from the side, which irritates this fish. When 
frightened, it moves around so its spine is aimed 
directly at the intruder, stinging with a darting, 
lightning-fast jab. 

Symptoms 

The sting of the scorpion fish causes an immediate 
severe stinging or throbbing pain, which may stay 
at the site of the wound or spread throughout the 
body and last for several hours or days. There may 
be redness and swelling at the site of the sting, and 
the area may become numb. The more dangerous 
varieties can cause loss of consciousness, paralysis, 
delirium, and convulsions, leading to fatal cardiac 
arrest. The profound pain, convulsions, paralysis, 
and unconsciousness — which can be immediate — 
can cause drowning. In addition, there is often a 
secondary infection and a fluctuating fever. 

Treatment 

There is no known antidote, although stonefish 
antivenin may be administered. Contact medical 
help immediately; flush the wound with fresh- 
er salt water and then soak the affected area in 
hot water or put hot compresses on it. The water 



230 sea cucumber 



should be very hot (120°F) so that the heat will 
deactivate the poison. Continue applying hot water 
for an hour. Recovery from a scorpion fish sting 
may take months and leave a permanent scar. 
See also lionfish; stonefish. 

sea cucumber (Holothurioidea class) Although 
sea cucumbers under most circumstances are safe 
to eat, there are toxic species that are difficult to 
identify. In addition, some species of sea cucumbers 
produce a poison that is quite toxic and can cause 
burning and inflammation on human skin and 
blindness if it comes in contact with the eyes. 

The toxin is located in tubules within the crea- 
ture's body, from which it can be excreted, forming 
long, sticky threads that can capture and trap an 
attacker. 

Poisonous part 

The toxin is called holothurin. 

Symptoms 

While little is known of the symptoms produced by 
poisonous sea cucumbers, eating the toxic species 
can be fatal. However, such intoxications are rare. 
Contact with hquid ejected from some sea cucum- 
bers may cause rash or bhndness. 

Treatment 

There is no known antidote. Treatment is 
symptomatic. 

sea snake (Hydrophidae) Considered by the Guin- 
ness Book of World Records to be the most venomous 
snake in the world, the sea snake has highly toxic 
venom — in some cases, more than 50 times as 
deadly as that of the king cobra. Of the 50 cata- 
loged species of sea snakes, all are venomous, and 
as many as 25 percent of their victims will die. 

Sea snakes inhabit the Pacific and Indian Oceans 
and are widely found around the Ashmore Reef in 
the Timor Sea off the coast of northwestern Aus- 
tralia. None have ever been found in the Atlantic 
Ocean or the Mediterranean or Red Seas. Huge 
clumps of many thousands of sea snakes may 
sometimes be found at sea; some experts believe 



this is because small fish often swim in shoals 
beneath floating debris. 

True snakes, the Hydrophidae have hdless eyes 
and a forked tongue, growing an average of four 
feet long. They are very well adapted to life in 
the sea, with a streamlined body, nostrils on top 
of their heads and special glands that excrete salt. 
Reports conflict as to whether these snakes are 
considered to be docile or aggressive. They have 
long been killed for their leather. 

Fortunately, however, the mechanism for 
injecting poison is not well developed in the sea 
snakes, and their fangs are very small. While it 
is often believed that these snakes have small 
mouths and can only bite a human's tender skin 
at the base of the thumb, this is not true. Many 
pearl divers in the Persian Gulf who weren't 
wearing goggles have died after accidentally grab- 
bing sea snakes. 

Poisonous sea snakes include the banded, or 
annulated, sea snake (Hydrophis cyanocinctus) :heaked 
sea snake (Enhydrina schistosa): yellow-lipped sea 
krait (Laticauda colubrina); olive-brown sea snake 
(Aipysurus laevis); yellow sea snake (Hydrophis spira- 
lis); Hardwicke's sea snake (Lapemis hardwickii); and 
the pelagic sea snake (Pelamis platurus). The largest 
species is Laticauda semifasciata; the sea snakes of 
this species gather together in groups numbering 
in the thousands to breed in the large coastal caves 
of Gato north of Cebu. Some species, such as the 
Laticauda colubrina, live partly on land, entering 
the water occasionally, although they are well 
equipped for life in the sea. 

Of all the sea snakes, the beaked sea snake is the 
most venomous and is responsible for more fatali- 
ties than all other sea snakes combined. The yellow 
sea snake and the Hardwicke's sea snake are not 
nearly as venomous, although both have caused 
several fatalities. The pelagic sea snake is the most 
common and least toxic, found on the west coast of 
the American tropics. 

In general, however, sea snakes are fairly inof- 
fensive and pose no great threat to humans, despite 
the toxicity of their venom. 

Poisonous part 

The extremely toxic venom is a neurotoxin that 
affects the muscles and paralyzes the nervous sys- 



sea wasp 231 



tern, causing the release of the protein myoglobin, 
which stains the urine red, damages the kidneys, 
and affects the heart. 

Symptoms 

Unlike the bite of many other poisonous sea 
creatures, the bite of a sea snake seems hke a 
harmless pinprick. Because symptoms appear very 
slowly — between 20 minutes and eight hours — the 
victim often does not connect the snakebite with 
subsequent symptoms. First, the victim feels weak- 
ness and then pain in the skeletal muscles. Victims 
notice numbness and thickening of the tongue 
and mouth, blurred vision, and difficulty in swal- 
lowing. Weakness increases, the eyelids droop, the 
jaws stiffen, and the pulse weakens and becomes 
irregular. Sometimes, nausea and vomiting are 
present. In cases of severe poisoning, symptoms 
worsen and cyanosis appears, followed by breath- 
ing problems and convulsions. Death may come in 
a few hours to a few days. 

Treatment 

Antivenin is available; the snake should be cap- 
tured and identified to rule out the bite of a 
harmless water snake. Cortisone or epinephrine 
is sometimes given to prevent anaphylaxis, and 
fluids and electrolyte levels are monitored. If a 
person has not been severely bitten, recovery is 
rapid. 

See also cobra, king; snakes, poisonous. 

sea urchin (Diadema setosum; Toxpneustes ele- 
gans; Asthenosoma jimoni) Of all the sea urchins, 
the sting from the long-spined variety (D. setosum) 
is the most poisonous. Red sea urchins T. elegans 
and A. jimoni are less venomous. Sea urchins are 
commonly found in warm waters around rocks or 
wrecks, where they can sting swimmers or divers 
even through shoes and gloves. They are rounded, 
about the size of a golf or tennis ball, with sharp 
spines radiating outward. 

Poisonous part 

Sea urchins have venomous spines with poisoned 
tips, and three pronged biting teeth that are 
extremely tenacious. 



Symptoms 

Although death is rare, the sting of the sea urchin 
penetrates soft tissue, causing an immediate severe 
stinging or throbbing pain, which may stay at the 
site of the wound or spread throughout the body 
and last for several hours or days. There may be 
redness and swelling at the site of the sting, and 
the area may become numb, followed by muscle 
weakness and possible paralysis. 

Treatment 

Contact medical help immediately. Remove spines; 
if the brittle tips break off and are not absorbed 
in two days, surgery may be required to remove 
them. Flush the wound with fresh- or salt water, 
and then soak the affected area in hot water or put 
hot compresses on it. The water should be very hot 
(I22°F) so that the heat will deactivate the poison. 
Continue applying hot water for 30 minutes to an 
hour. Have the victim lie still with the stung part 
immobile and lower than the heart. Tie a flat strip 
of cloth snugly around a stung arm or leg two to 
four inches above the sting, loose enough to allow 
a pulse farther out on the limb. Check periodically 
and loosen if necessary, but do not remove it. If 
swelling reaches the band, tie another band two 
to four inches higher up and remove the first one. 
There may be a purple stain on the skin around the 
wound, which is merely a pigment of the spine and 
not dangerous. 

sea wasp (Chironex fleckeri; Chiropsalmus quadri- 
gatus) One of the most venomous of the jellyfish, 
the sea wasp lives in warm water from Queensland 
northward to Malaya but also in cooler waters 
as far north as the central Atlantic seaboard; the 
Australian species is the most dangerous. Their 
tentacles may grow as long as 200 feet, although 
contact with only 20 feet of tentacle will be fatal. 
Sea wasps can be found close to shore, sometimes 
in only a few feet of water. 

A moderate sting from a sea wasp can be fatal 
in a few minutes. The sea wasp is considered to 
be one of the most deadly organisms in the world, 
and in Australia alone it has caused more than 50 
deaths in 20 years. In fact, the venom is so toxic 
that in laboratory experiments a solution diluted 



232 Seconal 



10,000 times still killed the animal before the 
syringe could be extracted. 

The only protection against the sting of sea wasp 
is the wearing of tights, which the wasps cannot 
penetrate; all life-saving teams in Queensland are 
required to wear them for this reason. 

Poisonous part 

The sea wasp's tentacles cluster at the corners of its 
body, and the stinging capsules within each con- 
tain a minute amount of one of the most deadly 
venoms ever discovered. The live nematocysts 
that contain the poison can live for months on 
the beach, if occasionally moistened with seawa- 
ter, and are capable of injecting the poison; even 
nematocysts that have been dried on the beach for 
several weeks maintain potency. 

Symptoms 

The sting of the sea wasp can be fatal within sec- 
onds. In general, there are painful swellings and 
purple-brown wheals at the site of the sting, which 
later necrose. Pain is said to be excruciating and 
can cause the victim to become distraught and 
irrational. Symptoms include muscular spasms, 
breathing problems, rapid and weak pulse, pulmo- 
nary edema, shock, and respiratory failure followed 
almost always by death, within 30 seconds to three 
hours; in general, death occurs within 1 5 minutes. 
Even the mildest sting is not pleasant, with acute 
burning pain and a wheal that lasts for months. 

Treatment 

There is not usually time to administer first aid or 
an antidote, although a sea wasp antivenin is avail- 
able in Australia. Stings from the sea wasp do not 
occur in the United States. 
See also jellyfish. 



Seconal See barbiturates. 



selective serotonin reuptake inhibitors (SSRIs) 

This class of antidepressants was first introduced 
in 1987 with the marketing of fluoxetine (Pro- 
zac). Experts believe that selective serotonin reup- 
take inhibitors (SSRIs) help relieve depression by 



blocking the reabsorption (reuptake) of a brain 
chemical called serotonin, which is associated with 
depression, behavior, and mood. SSRIs allow more 
serotonin to remain in the brain, which in turn 
improves mood. 

SSRIs are available in extended-release or con- 
troUed-release form, which provides the medica- 
tion throughout a day or for a week at a time 
with a single dose. The SSRIs approved by the 
Food and Drug Administration to treat depression 
include citalopram (Celexa), escitalopram (Lexa- 
pro), fluoxetine (Prozac), fluvoxamine (Luvox), 
paroxetine (Paxil), and sertraline (Zoloft). Some of 
these drugs are also used to treat conditions other 
than depression. 

Compared with other classes of antidepressants, 
SSRIs are generally less likely to have adverse 
interactions with other medications, and they are 
less dangerous if taken as an overdose. 

Symptoms 

An overdose of SSRIs rarely results in fatalities 
but in some cases causes a life-threatening condi- 
tion called serotonin syndrome, in which danger- 
ously high levels of serotonin accumulate in the 
brain. This syndrome can also occur when SSRIs 
are taken with other medications or supplements 
that have an influence on serotonin levels, such 
as monoamine oxidase inhibitors and St. John's 
wort. Signs and symptoms of serotonin syndrome 
include confusion, restlessness, hallucinations, 
extreme agitation, fluctuations in blood pressure, 
increased heart rate, nausea and vomiting, fever, 
seizures, and coma. 

In some cases, antidepressants may be associ- 
ated with worsening symptoms of depression or 
suicidal behavior or thoughts. These symptoms 
tend to appear early in treatment or when dosages 
are changed. 

Treatment 

If gastric lavage and/or charcoal are to be given, 
the airway must be clear. Gastric lavage is usually 
not necessary but may be performed within 60 
minutes of suspected ingestion. Activated char- 
coal can be administered if indicated. Seizures 
and muscular rigidity are best managed with 
benzodiazepines. 



shellfish poisoning 233 



selenium A metallic element found normally in 
the soil, selenium is necessary for human health 
but is toxic in large amounts, although few cases of 
selenium poisoning in humans have been reported. 
Selenium poisoning is more of a problem for farm 
animals and birds, although it can be a problem for 
farm families with wells polluted by runoff from 
selenium-rich agricultural soil. 

Selenium is used in a wide variety of products 
because of its ability to produce electricity when 
light is shined on it; it is widely used in photoelec- 
tric cells, light meters, photocopying machines, and 
other electrical components. It is also used to create 
the red color in warning lights, traffic lights, and 
brake lights. 

A well-balanced diet is the best way to obtain 
selenium; about two-thirds of dietary selenium 
comes from meat, fish, and dairy products, which 
provide enough selenium to satisfy daily require- 
ments but not enough to be toxic. 

Chronic poisoning may occur from numerous 
exposures during the manufacture of the wide 
range of products that use this element. 

Symptoms 

Chronic poisoning symptoms include pallor, garlicky 
odor to the breath, metallic taste, gastrointestinal 
disturbances, irritation of the nose, conjunctivitis, 
skin problems, drowsiness, and chest constriction. 

Treatment 

Removal from the environment and a selenium- 
free diet. 

shellfish poisoning Shellfish are highly suscep- 
tible to bacterial and viral contamination because 
they live close to the shore, where pollution tends 
to be worst. Cooking usually destroys the microbes 
that infect shellfish — but eating raw clams, oysters, 
and other shellfish is linked to nearly 1,000 cases 
of hepatitis alone each year. 

While shellfish by themselves are not poisonous, 
they can become contaminated by bacteria and 
other organisms from their environment and pass 
them on to humans when the shellfish is eaten. 
Oysters, clams, and mussels are particularly prone 
to becoming contaminated because of their meta- 



bolic system, which pumps water across the gills to 
isolate plankton for their food. This system makes 
them vulnerable to bacteria, viruses, or other con- 
taminants in the water. Lobsters and other crusta- 
cean shellfish only rarely become contaminated. 

In mussels, toxins are concentrated in the 
digestive glands, and toxicity is usually lost within 
weeks. But the Alaskan butter clam can remain 
toxic for up to two years after accumulating the 
toxin. However, the part of the mollusk that 
humans generally eat — the white meat, without 
the digestive glands — stores fairly small amounts 
of toxin. 

Seafood contaminated with toxins may look and 
taste normal, but normal cooking methods don't 
affect the toxin. State shellfish screening programs 
test shellfish for the presence of these toxins and 
monitor the safety of shellfish harvest beds. How- 
ever, people who catch their own shellfish from 
unapproved beds are at risk for a variety of toxic 
infections. 

The toxins may be produced as fish spoil (as in 
scombrotoxin) or as the by-products of toxic plank- 
ton (paralytic shellfish poisoning), or they may nat- 
urally be present in the fish itself (tetrodotoxin). 

Some types of plankton produce a toxin (saxi- 
toxin) that is eaten by shellfish along the North 
American coasts. These plankton multiply rapidly 
during the warm summer months; because their 
color is pink or red, this phenomenon has come to 
be called "red tide." When people eat shellfish con- 
taminated with the toxin, they can become very 
sick or die. It's not possible to build up immunity by 
becoming exposed to sublethal doses, and in some 
cases, the substance is so toxic that even one con- 
taminated shellfish can be fatal if eaten. This is why 
clams, oysters, and mussels are not sold during 
months without an r (the summer months — May, 
June, July, and August) . 

Shellfish poisoning caused by these toxic plank- 
ton comes in four forms: neurotoxic shellfish poi- 
soning (NSP), diarrheic shellfish poisoning (DSP), 
amnesic shellfish poisoning (ASP), and paralytic 
shellfish poisoning (PSP). Each has quite different 
etiology, symptoms and prognosis for recovery, 
but of the three, PSP is by far the most serious. 
All types are caused by 20 different toxins related 
to saxitoxin. The true incidence of these shellfish 



234 shigellosis 



poisonings is not known, because so many cases 
are believed not to be reported. 

Treatment 

There is no known antidote to saxitoxin. As in any 
treatment of curarelilte poisoning, administration 
of prostigmine may be effective, together with arti- 
ficial respiration and oxygen as needed. 

See also ciguatera; dinoflagellate; fish con- 
tamination; PARALYTIC SHELLFISH POISONING. 

shigellosis Shigellosis is caused by four different 
species of Shigella bacteria common in developing 
countries where lack of sewage treatment is linked 
to contaminated food and water. It is less common 
in the United States but still causes about 300,000 
cases each year. Shigellosis is very common among 
AIDS patients, and cases are most serious among 
them and among the very young and old. A person 
gets sick after ingesting bacteria, and only a few 
organisms can cause illness. A person is infectious 
from the time the diarrhea appears until the bacte- 
ria is no longer in the stool (about a month). 

Shigellosis is found in milk and dairy products, 
poultry, mixed salads (tuna, potato, shrimp, maca- 
roni, and chicken), and raw vegetables, but it can 
develop in any moist food that isn't thoroughly 
cooked. The bacteria multiply rapidly at room 
temperature. 

Symptoms 

Between eight hours to a week after eating tainted 
food or beverages, symptoms of nausea and vomit- 
ing, diarrhea, stomach cramps, weakness, vision 
problems, headache, and swallowing problems 
appear. Children or those with weakened immune 
systems may have more serious diarrhea. 

Diagnosis 

A culture of the stool will reveal the infection. 
Treatment 

Most people recover on their own, but some may 
need fluids to offset dehydration. Antibiotics will 
help stop the diarrhea, although Shigella is becom- 
ing resistant to some drugs. Antidiarrhea medica- 
tions should not be taken. 



Prevention 

Confirmed cases must be reported to the local 
health department, which will begin an investi- 
gation and control measures in order to prevent 
large-scale outbreaks. Although several vaccines 
have been tested, none has yet been licensed. The 
most important way to prevent the spread of this 
disease is to carefully wash your hands after using 
the toilet. 



sick building syndrome A condition in which 
people who occupy a building — most often either 
a place of employment or a home — experience 
acute health and comfort effects that appear to be 
associated with the time they spend in the building, 
but no specific cause or illness can be identified. 
The adverse effects may be limited to a particular 
room or area of the building or be widespread 
throughout the building. Symptoms may include 
headache, eye, nose, or throat irritation, dry cough, 
dry or itchy skin, dizziness, nausea, difficulty in 
concentrating, fatigue, and sensitivity to odors. 
Most people who suffer with this syndrome report 
that they get relief from their symptoms once they 
have been away from the building for some time. If 
the syndrome is associated with a place of employ- 
ment, people often feel better over the weekend 
and then get symptoms again at the beginning of 
the work week. 

Causes of or contributing factors to sick build- 
ing syndrome may include improper or inadequate 
ventilation. When national energy conservation 
measures were initiated as a result of the 1973 oil 
embargo, the amount of outdoor air provided for 
ventilation in buildings was reduced from 1 5 cubic 
feet per minute (cfm) to five cfm per building occu- 
pant. This reduction in air ventilation rates was not 
adequate to maintain the health and comfort of the 
building occupants. Another factor in sick building 
syndrome is ineffective heating, ventilating, and 
air-conditioning systems. 

Chemical contaminants from either indoor or 
outdoor sources may also be a cause of or contrib- 
uting factor in sick building syndrome. Indoor air 
pollution sources may include adhesives, carpet- 
ing, copy machines, manufactured wood products, 
tobacco smoke, and cleaning supplies that may 



silver nitrate 235 



emit volatile organic compounds (VOCs), including 
formaldehyde. Tobacco smoke contributes VOCs, 
other toxic compounds, and particulate matter. 
Combustion products such as carbon monoxide, 
nitrogen dioxide, and respirable particles can come 
from unvented stoves, fireplaces, and heaters. Out- 
door sources of chemical contaminants that can 
enter buildings include motor vehicle exhaust and 
pollutants from plumbing vents and sewer hues. 

Biological contaminants, such as bacteria, pol- 
len, viruses, and molds may breed in stagnant 
water that can accumulate in humidifiers, drain 
pans, and ducts, or where water has collected 
on carpeting, insulation, or ceiling tiles. Physical 
symptoms associated with biological contamination 
include cough, fever, chills, muscle aches, allergic 
reactions, and chest tightness. Legionnaire's disease 
and Pontiac fever are two similar conditions that 
are caused by a biological contaminant, the bacte- 
rium Legionella pneumophila. According to the Cen- 
ters for Disease Control and Prevention, between 
8,000 and 18,000 people are hospitalized each year 
with Legionnaire's disease, and it is believed the 
actual number is much greater because many cases 
are not diagnosed or reported. 

The most serious of the indoor air pollutants is 
carbon monoxide, which, according to the Con- 
sumer Product Safety Commission, causes more 
than 200 deaths a year. Dangerous levels of the 
odorless gas may be caused by automobile exhaust 
and improperly installed or vented appliances. 
The CPSC now recommends that all homes be 
equipped with carbon monoxide detectors (similar 
to smoke alarms) that will sound a warning when 
the gas reaches dangerous levels. 

See also carbon monoxide. 



sidewinder (Crotalus cerastes) Also known as the 
horned rattler, this is one of three rattlesnakes from 
the family Viperidae known for its quick sideways 
motion across the shifting desert floor. Its odd, 
sideways motion leaves a distinct trail of parallel 
J-shaped marks. 

The sidewinder has a distinctive look, with a 
prominent triangular, hornlike projection over 
each eye. The snake is found in arid deserts with 
mesquite-crowned sand hills throughout the south- 



western United States and northeastern Mexico. It 
is most often encountered as it crosses roads at 
night in the spring; during the day, it usually hides 
in burrows or bushes. 

Symptoms 

Symptoms appear within 15 minutes and include 
excessive thirst, nausea, vomiting, shock, paraly- 
sis, respiratory problems, anemia, necrosis, kidney 
problems, and sometimes death. The bite of a 
rattlesnake is painful. Indications of a serious bite 
include swelling above the elbows or knees within 
two hours, hemorrhages, numbness at the punc- 
ture site, tingling around the mouth, yellow vision, 
vomiting, and violent spasms. 

Treatment 

Antivenin is available. 

See also massasauga; pit vipers; rattlesnake, 
canebrake; rattlesnake, cascabel; rattlesnake, 

EASTERN DIAMONDBACK; RATTLESNAKE, MEXICAN 

west coast, rattlesnake, red diamondback; 
rattlesnakes; rattlesnake, timber; rattlesnake, 
western diamondback; snakes, poisonous; viper, 
gaboon; viper, jumping; viper, malayan pit; viper, 
RussEL's; VIPER, sawscaled; viper, Wagler's pit; 
vipers; water moccasin; wutu. 

silver nitrate This astringent is used primarily to 
prevent a serious form of conjunctivitis in new- 
borns and may also be used on burns and dress- 
ings. It dissolves readily in water and is fatal when 
ingested either in its salt form or as a hquid. 

Symptoms 

Immediately upon ingestion, silver nitrate causes 
pain and burning in the mouth, blackened skin, 
mucous membranes, throat and abdomen, vom- 
iting and diarrhea, collapse, shock, convulsions, 
coma, and death. Repeated doses over a long 
period of time will cause a permanent blue-black 
color in the skin. 

Treatment 

Treatment for poisoning should begin immediately 
after ingestion by washing out the stomach repeat- 
edly with I percent sodium chloride (salt) solution. 



236 sleeping pills 



After this lavage, administer a purgative, such as 30 
grams of sodium sulphate in 250 milliliters of water, 
which should remain in the stomach. Demulcents 
such as milk or egg white can be given with pethi- 
dine or morphine if necessary for pain. Pay close 
attention to fluid balance and kidney function. 

sleeping pills The term "sleeping pills" is a broad 
one, encompassing a wide variety of drugs from 
different classes, all of which are used to treat 
insomnia. These drugs may include benzodiaz- 
epines, nonbenzodiazepine sedative hypnotics, 
barbiturates, antidepressants, and antihistamines 
(found in most over-the-counter sleep aids). 

According to a 2005 National Institutes of 
Health conference statement, the antidepressant 
trazodone is the most commonly prescribed drug 
for treatment of insomnia in the Untied States, 
even though trazodone has not been officially 
approved by the Food and Drug Administra- 
tion (FDA) for treatment of insomnia. Drugs that 
have been approved by the FDA for insomnia 
include the benzodiazepines estazolam (ProSom), 
temezepam (Restoril), flurazepam (Dalmane), and 
quazepam (Doral); nonbenzodiazepines zaleplon 
(Sonata), Zolpidem (Ambien), and eszopiclone 
(Lunesta); ramelteon (Rozerem); and triazolam 
(Halcion). Some of the drugs are designed to help 
you fall asleep; others help you stay asleep. 

The rule of thumb with sleeping pills is to take 
the least amount needed to get relief and to taper off 
of them quickly to avoid getting addicted to them. 
People who use sleeping pills regularly over time 
often develop tolerance and usually need more and 
more of the drug to achieve the desired effect. 

Use of alcohol in combination with sleeping pills 
multiplies the effects. Other drugs, including those 
used to treat heart disease, diabetes, depression, 
and duodenal ulcers, may have an adverse impact 
on sleeping pills. 

Symptoms 

These depend on the type of drug taken, but typi- 
cally include slurred speech, lack of coordination, 
unsteady gait, euphoria or depression, impaired 
attention or memory. Heart and/or lung failure are 
also possible. 



Treatment 

Initiate immediate gastric lavage where appropriate 
along with general symptomatic measures. Intra- 
venous fluids should be administered as needed. 
Vital signs should be monitored and treated as 
appropriate. 

See also barbiturates; benzodiazepines; Dal- 
mane; ETHYL ALCOHOL. 

slug bait See metaldehyde. 

smooth-scaled snake (Parademansia micro- 
lepidotus) The most venomous land snake 
in the world, according to the Guinness Book of 
World Records, this snake is found in southwestern 
Queensland and northeastern South Austraha and 
Tasmania. Until 1976, it was thought to be a West- 
ern form of the taipan, but its venom is actually 
quite different. The smooth-scaled snake grows 
to up to six feet, six inches long, and its venom 
has been measured at 0.00385 ounces after milk- 
ing — enough to kill 125,000 mice. 

Symptoms 

Pain and swelling within 30 minutes, dilated 
pupils, and low blood pressure followed by muscle 
weakness and paralysis of breathing muscles. 

Treatment 

Antivenin is available. 

See also snakes, poisonous; taipan. 

snakes, poisonous There are about 3,000 species 
of snakes in the world, but only about 10 percent 
of them are poisonous. Venomous snakes come 
in all sizes, from the tiny desert vipers to the king 
cobra, growing up to 16 feet long; a king cobra, 
when angered, can rear up and stand as tall as a 
person. While there are many old folk methods to 
quickly determine if a snake is poisonous, such as 
counting the rows of scales, there is no practical 
way to tell the poisonous from the harmless. 

According to World Health Organization statis- 
tics, about 50,000 people throughout the world 
die from snakebites each year — mostly in India; 



snakes, poisonous 237 



about 8,000 victims are treated each year in the 
United States. The highest death rate from snake- 
bite in the United States is reported from Arizona, 
Florida, Georgia, Texas, and Alabama, in that order. 
According to the Guinness Book of World Records, 
Burma has the highest mortality rate — 15.4 deaths 
per 100,000 population each year. 

There are only four varieties of snakes in the 
United States that are poisonous — the rattlesnake, 
copperhead, water moccasin, and coral snake, 
but they are widely distributed throughout the 
country. The water moccasin is distributed over 
the Southwest, the Gulf states, and the Mississippi 
valley as far north as southern Illinois. Of all poi- 
sonous snakes, the copperhead is probably more 
commonly found throughout the country, espe- 
cially in North and South Carolina, West Virginia, 
Pennsylvania, Missouri, Oklahoma, Arkansas, and 
Illinois. Rattlesnakes are found throughout the 
continental United States. 

The coral snake is usually associated with the 
southern United States. Of the 115 species in this 
country, only about 20 are dangerous, including 16 
species of rattlesnakes. Generally, only the eastern 
and western diamondback, canebrake, timber, and 
Mojave rattlers (and a few subspecies) could be 
considered life threatening. Of these, diamondbacks 
are considered to be the most dangerous, because of 
their large size, the length of their fangs, the large 
quantity of venom and the nature of their venom. 

Rattlers account for about 65 percent of the ven- 
omous snakebites that occur in this country each 
year, and for nearly all of the nine to 15 deaths. A 
smaller fraction of bites comes from copperheads, 
fewer still from cottonmouths, and only three or 
four bites a year from coral snakes. Many snakebite 
victims are children or members of religious sects 
that handle deadly snakes. 

Poisonous part 

Scientists have identified more than 100 proteins 
in rattlesnake venom, including deadly neurotoxic 
compounds that dissolve cells and damage blood 
vessels. Heart and kidney complications often fol- 
low. Most snakebite fatalities occur 18 to 32 hours 
after a bite, but death can occur within 60 minutes 
or after several days. Some snakes (such as cobras) 
lay eggs, while others (such as vipers) give birth to 



live young. Newly born venomous snakes are just 
as dangerous as their parents and can often be far 
more aggressive than the old folks; baby cobras, in 
particular, are vicious and will strike even while 
they are emerging from their eggs. 

Symptoms 

Fang marks and possibly teeth marks may be vis- 
ible. Symptoms include an immediate, burning 
pain that spreads rapidly (especially with a pit 
viper's bite), and sudden swelling beginning soon 
after the bite in the bite area and then spread- 
ing throughout the body. (This is especially true 
for bites on the arm or leg.) Systemic symptoms 
include shock, nausea, weakness, and numbness; 
muscles may twitch and skin may tingle. There 
are a number of factors that influence the severity 
of a snakebite: the amount of venom injected; the 
size and species of the individual snake; the age, 
size, health, and sensitivity of the victim; the types 
of clothing worn; and the position and number of 
bites inflicted. If an hour passes after a snakebite 
and no symptoms appear, chances are not enough 
venom was injected and the danger is slight. 

Treatment 

Despite the long history of snakebites and their treat- 
ment, the problem of how to deal with snakebites 
remains controversial: ice or no ice? Tourniquet or 
constriction band? Cut and suck or not? More than 
200 different first aid procedures for snakebite have 
been recommended by various experts. 

The emphasis on treating a snakebite should be 
placed on getting prompt medical care, and first 
aid should never be considered to be a substitute 
for antivenin. Rapid treatment with an antivenin 
can help a snakebite victim regardless of whether 
or not the bite would have been fatal. Without 
antivenin treatment, hospital stays for venomous 
snake bites last about twice as long. The venom of 
all snakes in the Crotahdae family (rattlesnakes, 
copperheads, and water moccasins) contains simi- 
lar poisons, and all can be treated with antivenin. 
A bite from the eastern coral snake requires a sepa- 
rate antivenin, and there is no antivenin for the 
western coral snake. 

In addition, there are different types of venom, 
and it is useless to treat a victim with an antivenin 



238 sodium bicarbonate 



for viper bites if the injury was caused by a cobra. 
And venom even differs among specimens from 
different areas, even within the same species; for 
example, antivenin from an Indian member of a 
particular species will not be very helpful against 
bites of Thai cobras of the species. 

Here's what to do if someone is bitten by a ven- 
omous snake. 

• Apply a pressure bandage over the bite site and 
on as much of the affected limb as possible. 

• Immobilize the affected limb, using a splint if 
possible. 

• Both pressure and immobihzation are required. 

• Reassure patient and arrange transport to near- 
est hospital without delay. 

• Advise hospital of the impending arrival; main- 
tain contact with hospital while transporting the 
patient. 

• If paralysis occurs rapidly and breathing 
becomes labored or ceases, try mouth-to-mouth 
resuscitation. 

• If blood pressure falls (patient feels faint or loses 
consciousness) elevate legs. 

• Keep airway clear of secretions at all times. 

And here's what NOT to do if bitten by a venom- 
ous snake. 

• Do not try to kill or catch the snake for 
identification 

• Do not wash the bite site (surface venom resi- 
dues can be used in venom detection kits). 

• Do not release the pressure bandage (hospital 
staff will decide when this is appropriate). 

• Do not use cold/ice pack. 

• Do not give the patient any beverages or food. 

• Do not use any medication. 

• Do not apply tight, narrow constricting bands. 

• Do not use any form of electrical shock treatment. 

Cutting into a snakebite is controversial. If you 
are trained, have the right equipment and are far 
from medical help, you can incise a snakebite. Treat 



for shock and be prepared to give artificial respira- 
tion if breathing stops, if you are trained in CPR. 
Have someone phone ahead to alert the hospital, 
identifying the type of snake if possible (or take the 
dead snake with you). 

Precautions 

When moving through a snake -infested area, hik- 
ers should watch the path and never put feet or 
hands where they can't be seen. If walking through 
tall grass or bushes, poke the clumps with a stick 
to warn snakes. Do not reach above your head 
or put hands into crevices. Since about half of 
all snake strikes are below the knee, wear heavy, 
leather, high-top shoes or boots and loose-fitting 
long pants, with cuffs reaching over the tops of the 
shoes. When camping, avoid areas near rocks, logs, 
burrows, or caves. Always wear heavy gloves when 
cleaning up debris — especially logs or old lumber, 
and use a crowbar to move them. 

Snakes are more dangerous during early spring; 
they've been storing venom and the poison glands 
are full. If a snake is spotted, back away from it for 
at least two to three feet. Snakes can strike about 
half their body length (and most are less than five 
feet long). 

See also adder; adder, common; adder, puff; 

BLACK snake, AUSTRALIAN; BOOMSLANG; BROWN 

snake; bushmaster; coral snake; coral snake, 
Arizona; coral snake, eastern; habu, Okinawa; 
KRAiT, blue; mambas; massasauga; pit vipers; 
rattlesnake, cascabel; rattlesnake, eastern dia- 
mondback; rattlesnake, Mexican west coast, 
rattlesnake, red diamondback; rattlesnake, tim- 
BER; rattlesnake, western DIAMONDBACK; RATTLE- 
SNAKES; SIDEWINDER; SMOOTH-SCALED SNAKE; VIPER, 
GABOON; VIPER, JUMPING; VIPER, MALAYAN PIT; VIPER, 

RussEL's; VIPER, sawscaled; water moccasin; 

WUTU. 



sodium bicarbonate This buffering agent is used 
in the treatment of poisoning by methanol, ethyl- 
ene glycol, or salicylate. It counteracts metabolic 
acidosis and enhances the ehmination of salicy- 
late or phenobarbital. It also helps to treat heart 
problems resulting from overdoses of cyclic anti- 
depressants and some antiarrhythmic drugs. Used 



spiders, poisonous 239 



in gastric lavage solution, it can be helpful in the 
treatment of excessive iron ingestion. 

sodium carbonate See alkaline corrosives. 



sodium fluoroacetate See compound 1080. 



sodium hydroxide See lye. 

sodium hypochlorite The most common form of 
the active ingredient in bleach. 
See also alkaline corrosives. 



sodium phosphate See alkaline corrosives. 
solanine See potato. 



solvent abuse Certain volatile liquids give off 
intoxicating fumes that, when sniffed, produce an 
effect similar to getting "high" on drugs or alcohol. 
Glue sniffing is the most common form of solvent 
abuse, but many other substances are used (espe- 
cially those containing toluene or acetone). 

The solvent is usually sniffed from a plastic bag 
containing the solvent, although sometimes aero- 
sols are sprayed into the nose or mouth. The prac- 
tice is often a group activity that usually lasts only 
for a few months at a time. However, solitary abuse 
is much more serious and may last for a much lon- 
ger period of time. 

Symptoms 

Inhaling solvent fumes may cause hallucinations; 
chronic abuse may cause headache, vomiting, stu- 
por, confusion, and coma. Death may occur as the 
result of a direct toxic effect on the heart, from a 
fall, choking on vomit, or asphyxiation due to the 
clinging bag around the nose and mouth. Other, 
long-term effects include damage to the membrane 
lining of the nose and throat, the kidneys, the liver, 
and the nervous system. The signs of solvent abuse 



include intoxicated behavior, flushed face, mouth 
ulcers, solvent smell, and personality changes. 

Treatment 

Maintain airway, administer supplemental oxygen, 
and monitor blood gases and chest X-rays. Treat 
symptoms of coughing and coma and broncho- 
spasm if they occur. Avoid the use of epinephrine 
because of the risk of aggravating arrhythmias. 
See also trichloroethane; trichloroethylene. 

South American rattlesnake See rattlesnake, 
cascabel. 



spathiphyllum (Spathiphyllum) Also known as 
the peace plant, this is an extremely common 
indoor potted plant popular as a commercial indoor 
landscape plant because of its limited light require- 
ments. These plants, which can reach about two 
feet in height, produce a single white or greenish 
flower with a white spadix resembling a small ear 
of corn. 

Poisonous part 

All parts of this plant are toxic and contain water- 
insoluble raphides of calcium oxalate. 

Symptoms 

Upon ingestion, burning, swelling, and pain of the 
lips, mouth, tongue, and pharynx; because of this 
immediate pain, large amounts of this plant are not 
usually eaten. Contact dermatitis may be caused by 
the root juices. 

Treatment 

Cool liquids, including milk, held in the mouth and 
analgesics may ease the pain. 
See also oxalates. 

spiders, poisonous Although most of the more 
than 50,000 species of spiders found in the United 
States actually possess poison glands connected to 
their fangs, only a very few are capable of piercing 
human skin. Those that can include the black widow 
(Latrodectus), the brown recluse spider (Loxosceles), 



240 spindle tree 



the jumping spider (Phidippus), and the tarantula (a 
common name given to many large spiders). 

In general, most spider attacks occur when 
someone disturbs a spider's nest while working 
outdoors or making house repairs. 

See also black widow spider; brown recluse 
spider; tarantula. 

spindle tree (Euonymus europaeus) This small 
tree has branches close to the ground and thin gray 
bark, looking very similar to its close cousin burn- 
ing bush (E. atropurpureus), except that its flowers 
are yellow-green. Introduced from Europe, this 
tree spread from cultivation in iVIassachusetts to 
Wisconsin and south. 

Poisonous part 

The leaves, seeds, and bark of this tree contain the 
cardiac glycoside evomonoside, similar to digitalis; 
a group of alkaloids, including evonine, that have 
not been evaluated; and a protein that inhibits pro- 
tein synthesis in intact cells. 

Symptoms 

Within 10 to 12 hours, ingestion results in symp- 
toms similar to those of meningitis: watery, bloody 
diarrhea; colic; vomiting; fever and convulsions; and 
liver damage that can be fatal within eight hours. 

Treatment 

Recommendation for treatment is difficult, since 
the underlying toxin is unknown. Replace fluids 
and electrolytes. 

See also cardiac glycosides. 

spurge nettle (Cnidolscolus stimulosus) A peren- 
nial herb that is native to southeastern North 
America and also found in Europe and Asia. Spurge 
nettle, which is also known as "tread-softly," is cov- 
ered with stinging hairs. It inflicts a painful sting 
on contact with the skin and can be poisonous to 
some people. 

Poisonous part 

Its toxin includes toxalbumins and cathartic oils. It 
can also cause skin reactions. 



Symptoms 

Contact produces instant, intense stinging and itch- 
ing because of an irritating substance injected into 
the skin by the plant's stinging hairs, and causes a 
skin rash that disappears in about 30 minutes. A 
dull purple stain on the skin may linger for several 
weeks. 

Treatment 

Symptomatic. 

squill (Scilla) [Other names: Cuban lily, hyacinth- 
of-Peru, sea onion, star hyacinth.] This hyacinth 
look-ahke is found as a hardy perennial in the 
north temperate zones to southern Canada. It is 
often grown for its attractive blue, purple, or white 
flowers. 

Poisonous part 
The whole squill plant is poisonous and contains 
digitalishke glycosides. 

Symptoms 

There is a variable latency period between inges- 
tion and symptoms, depending on the amount 
of the plant eaten. When they appear, symptoms 
include pain in the mouth, lips, tongue, and throat, 
nausea and vomiting, abdominal pain, cramps and 
diarrhea, hyperkalemia, and heart disturbances. 

Treatment 

Gastric lavage followed by the administration of 
activated charcoal and saline cathartics. Monitoring 
of potassium levels and electrocardiogram should 
be performed. In the event of heart problems: 
administration of atropine for conduction defects; 
phenytoin for rhythm disturbances. 
See also digitalis. 



staphylococcus enterotoxin One of the most 
common types of food poisoning in the United 
States, affecting almost everyone at least once. 
Although the bacteria are easily destroyed by high 
heat during cooking, they also produce a heat- 
resistant toxin. It is believed that only a few strains 
of staphylococci produce enterotoxins, which may 



star-potato vine 241 



occur in a wide variety of foods (sucfi as milk, 
cheese, ice cream, cream-filled bakery goods, dried 
beef, sausage, or chicken gravy). Poisoning with 
this type of bacteria most often occurs after eating 
food that has been kept warm for several hours 
before being served. In addition, food may be con- 
taminated from infected food handlers. 

Staphylococcus enterotoxin may be suspected 
when there has been only a brief interval between 
eating suspected tainted food and the onset of 
symptoms. It can be confimed by bacteriological 
examination for the presence of staphylococci; 
enterotoxin may also be produced by staphy- 
lococci in persons treated with broad-spectrum 
antibiotics. 

The best way to prevent this type of food poi- 
soning is to refrigerate perishable foods adequately. 
While heat does destroy the bacteria, it does not 
destroy the enterotoxin. 

Symptoms 

Symptoms usually appear within three hours of 
eating the tainted food; the incubation period 
depends on the amount of food eaten and the 
susceptibility of the consumer. (The aged, immu- 
nocompromised, and the very young are the most 
vulnerable.) Symptoms begin with salivation, fol- 
lowed by nausea, vomiting, abdominal cramps, 
prostration, and diarrhea; in severe poisoning, vic- 
tims experience marked prostration together with 
vomiting, diarrhea, and sometimes, shock. Symp- 
toms usually fade after five to six hours, although 
a few fatal cases have been reported among vulner- 
able populations. 

Treatment 

Significant loss of fluids and disruption of electro- 
lyte balance may require parenteral administration 
of fluids and electrolytes; treatment for shock may 
be required following significant loss of fluids. 

star of Bethlehem (Ornithogalum umbellatum; 
"wonder flower" — O. thyrosides) [Other names: 
African wonder flower, chincherinchee, dove's 
dung, nap at noon, summer snowflake, wonder 
flower.] Found in warm climates, the flower of 
the Bible has creamy white, starlike flowers on 



upright slender stems that may reach two feet in 
height, and long, narrow leaves with onionlike 
bulbs. Found primarily in the Middle East, both 
species are also kept indoors and sold by florists as 
a cut flower. 0. umbellatum has been naturalized in 
the southeastern United States, in iVIississippi, Mis- 
souri, Kansas, and eastward. 

Poisonous part 

All parts of the star of Bethlehem plant are toxic, 
especially the onionlike bulb; the poisons are con- 
vallatoxin and convalloside (the same as hly of the 
valley) plus cardiac glycosides. 

Symptoms 

Immediately after ingestion, symptoms begin: 
shortness of breath, irritation of the mouth and 
throat, nausea, vomiting, abdominal pain, diar- 
rhea, and respiratory problems. Fatalities have 
been reported from ingesting this plant. 

Treatment 

Gastric lavage and treatment of symptoms, fol- 
lowed by the administration of activated charcoal 
and saline cathartics. Electrocardiogram and potas- 
sium levels should be monitored repeatedly. 

See also cardiac glycosides; lily of the valley. 

star-potato vine (Solanum seaforthianum) Some- 
times called the Brazilian nightshade, this South 
American plant is also cultivated in warmer areas 
in Florida and Hawaii. It is a member of a very large 
genus with 1,700 species, most of which have not 
been evaluated toxicologically. 

Poisonous part 

Human poisoning is usually attributed to imma- 
ture fruit, which contains the toxin solanine 
glycoalkaloid. 

Symptoms 

While there is little danger of fatal poisoning in 
adults, children may ingest a fatal amount of this 
plant. Symptoms appear several hours after inges- 
tion and include gastric irritation, scratchy throat, 
fever, and diarrhea (solanine poisoning is often 
confused with bacterial gastroenteritis). 



242 Stelazine 



Treatment 

The same general supportive care that would be 
given in gastroenteritis cases; fluid replacement 
may be required. 

Stelazine (trifluroperazine) This is one of the psy- 
chometric drugs used to treat psychotic anxiety and 
agitated depression. It is available as a tablet, hquid, 
or injection and works by depressing the central 
nervous system. 

Symptoms 

Within 20 minutes after an overdose, Stelazine 
causes agitation, convulsions, fever, low blood 
pressure, coma, and cardiac arrest. 

Treatment 

Do not induce vomiting; perform gastric lavage and 
administer Cogentin; treat other symptoms as they 
appear. 

See also antidepressants. 



stingray (Urobatis halleri, Dasyatis longus, etc.) 

More than 1,500 cases of stingray attacks are 
reported in the United States each year, usually 
caused when a swimmer inadvertently steps on a 
stingray buried in the mud or sand. The Dasyatis 
stingrays are particularly noted for burying them- 
selves in the mud or sand. When trod upon, the 
stingray flings its tail up and forward, burying the 
stinger in the victim's foot. 

A stingray will never attack humans — fleeing if 
approached — unless it perceives itself under attack. 
When threatened, it can whip its tail around until 
it finds its attacker. It is possible to drive away 
stingrays by shuffling the feet in murky water. 

Stingrays are found throughout the world and 
include the diamond, butterfly, European, eagle, 
California, and South American freshwater sting- 
ray. All large varieties found in freshwater are dan- 
gerous. Many stingrays do not travel far from their 
own area, seeming to display a sense of territory. 

Poisonous part 

The fearsome whiphke tail of the stingray is longer 
than its body, and near the base of its tail it has 



one, two, or three flattened barbed spines with 
small, sharp teeth connected to a poison sac; the 
barbs point backward, making it difficult to remove 
the barb after penetration. The tail is coated with 
venomous slime that can cause serious injury or 
even death to humans. Often, the entire stinger 
is left embedded in the wound, and pulling it out 
may further damage surrounding skin. When the 
spine stabs into the skin, it tears the sheath around 
the spine, which releases the venom, producing a 
violent reaction in the skin tissue. Some varieties of 
stingrays can inflict such a deep wound that they 
can transmit the tetanus bacilli, causing tetanus 
in their victims. The stingray venom is one of the 
most powerful vasoconstrictors among all the ani- 
mal toxins and is markedly unstable. It has caused 
coronary vessel and resultant heart damage in ani- 
mal experiments. 

Symptoms 

While death is rare, the sting of the stingray causes 
an immediate severe stinging or throbbing pain, 
which may stay at the site of the wound or spread 
throughout the body and last for several hours or 
days. Most stingray wounds are found on the ankle 
or foot and may be more of a laceration than a 
wound. There may be redness and swelling at the 
site of the sting, and the area may become numb, 
followed by dizziness, weakness, cramps, sweating, 
and falling blood pressure. Fatalities have been 
reported when the barb enters the chest or abdo- 
men, but they are rare. 

Treatment 

There is no known antidote. Contact medical help 
immediately; flush the wound with salt water and 
then soak the affected area in hot water for one 
hour. The water should be very hot (122°F), so 
that the heat will deactivate the poison and also 
ease pain. Pain medication may be administered, 
and lacerations are surgically closed. Generally, 
victims recover within 48 hours, although hos- 
pitalization may be needed for those with persis- 
tent symptoms of chest pain, irregular pulse, or 
hypotension. Victims who have been stung on 
the chest or abdomen may require exploratory 
surgery. Tetanus shots and antibiotics are also 
necessary. 



strychnine 243 



stonefish (Synanceja horrida) One of the world's 
most virulent animals, t